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INTERNATIONAL SALES AND DISTRIBUTION MANAGER FOR BIOMEDICA
IMMUNOASSAYS (M/F/D)

Are you ready to take the next step in international Life Science sales? We are looking for an “International Sales and Distribution Manager” to join the Biomedica Immunoassays team in Bratislava, Slovakia, starting March 2026.

About Biomedica

Biomedica Slovakia is part of the Biomedica Group headquartered in Vienna, Austria. We have been on the forefront as a distributor of medical devices, in vitro diagnostics, products for Life Sciences, and Clinical IT for more than 40 years.

About Biomedica Immunoassays

Biomedica Immunoassays develops and produces internationally recognized high-quality ELISA kits used by leading scientific institutions, CROs, and pharmaceutical laboratories worldwide.

We started our own R&D programme in 1988 and now produce a range of innovative and high-quality immunoassays for clinical research in the field of cardiorenal diseases as well as mineral and bone disorders.

We are setting the standard for clinical research using serum-based calibrators and controls, thus enabling researchers to collect biologically reliable data. The supplied immunoassays are validated following international quality guidelines.

For specific markers, Biomedica has become a market leader with a continuously growing portfolio. A worldwide distribution network has been established for these products as well as an analytical testing service, which offers customers in-house analysis of their samples.

Are you ready to take the next step in international Life Science?

We are looking to strengthen our team with an

INTERNATIONAL SALES AND DISTRIBUTION MANAGER FOR BIOMEDICA IMMUNOASSAYS (M/F/D)

located in Bratislava, Slovakia. Full-time, starting March 2026

 

Your responsibilities

 

• Manage an international distribution network
• Provide technical support of distributors and end-users with product specific information
• Build and maintain relationships with key international customers
• Provide end-clients with customized quotations, negotiating contracts and oversee logistics and export documentation
• Drive market expansion by identifying new opportunities, emerging markets and new segments
• Monitor competitors and market prices
• Collect and analyse customer feedback
• Participation in international congresses, symposia and exhibitions
• Budget and sales planning in a cooperation with responsible manager
• Support production in creating production plans
• Handle complaints and troubleshoot in cooperation with the laboratory team

 

Your profile

 

• Bachelor’s degree, Master’s degree or Postgraduate in biology, chemistry, biotechnology or a related field
• Experience in international sales or distribution management
• Language skills: English – fluency in spoken and written
• Strong self-organization and ability to work independently
• Strong negotiation and cross- cultural communication and presentation skills
• Friendly and polite behaviour
• High social competence and team spirit
• Willingness to learn
• Flexibility and willingness to travel (travel activity up to approx. 20%, driving license B required)
• Microsoft Office skills

 

We offer

 

• Long-term employment in a well-known and growing international company
• Full time job
• Good company atmosphere
• Independent working
• Established product line of high quality
• Intensive training opportunities
• Company notebook and mobile phone
• Competitive salary based on individual agreement
• Attractive bonus system

 

The gross monthly salary for this position starts at EUR 2,000 (full-time) and will be discussed and agreed on an individual basis, depending on qualifications and professional experience.

 

Informationt about the selection process

 

This is a unique opportunity to join an innovative international company in a growing industry that can provide career security and genuine advancement opportunities for those who show potential.

We are seeking candidates with initial experience in international sales and distribution management within the life science industry. In managing relationships with our distributors and end-clients, you should demonstrate excellent communication and presentation skills, along with the ability to interact effectively with diverse cultures and personalities.

We look forward to receiving your written application (your CV and letter of motivation).

Please send your application by email to petra.bafrncova@bmgrp.sk

Join us and make a difference!

Worldwide, cardiovascular diseases (CVDs) are the primary cause of mortality (1). They involve a variety of underlying mechanisms, with increased oxidative stress being one of the key contributing factors.

Behavioral risk factors like poor diet, lack of physical activity, and tobacco use are connected to CVDs. Conditions that heighten the risk include obesity, high blood sugar, hypertension, increased low-density lipoprotein (LDL) cholesterol, and oxidative stress (1).

Understanding oxidative stress

 

Oxidative stress occurs when there is an imbalance between the production of free radicals (reactive oxygen species – ROS) and the body’s antioxidant defenses (endogenous antioxidant capacity) (2). ROS are by-products of cellular metabolism and can be triggered by various factors such as pollutants, heavy metals, tobacco, drugs, and others. It is believed that oxidative stress plays a role in the development and progression of numerous diseases, including cancer (3), diabetes (4), metabolic syndrome (5), Alzheimer´s disease (6), atherosclerosis (7), and cardiovascular conditions (8).

Biomarkers of Oxidative Stress in Cardiovascular Diseases

Oxidized LDL (oxLDL) and Autoantibodies Against Oxidized LDL

Atherosclerosis is a disease characterized by the accumulation of lipids, fibrous tissue, and calcification in large arteries. The process starts with endothelial activation, followed by a series of events that result in vessel narrowing and the activation of inflammatory pathways, leading to the formation of atheromatous plaques. These mechanisms collectively contribute to cardiovascular complications (9).

Oxidized LDL (OxLDL) and anti-OxLDL antibodies are closely linked and play crucial roles in the development of atherosclerosis, contributing to plaque formation, inflammation, and rupture. While OxLDL encourages foam cell development, anti-OxLDL antibodies, may provide a protective effect against coronary artery disease (CAD). Both are promising candidates as diagnostic biomarkers and targets for imaging in assessing cardiovascular risk (10).

Autoantibodies targeting oxidatively modified LDL (anti-oxLDL Ab) have been identified in both patients with atherosclerosis and healthy individuals. It is proposed that these antibodies reflect ongoing oxidation processes occurring within the body.

Anti-oxLDL Ab levels can be quantified in human blood samples using a standard ELISA assay . Several studies suggest that autoantibodies to oxLDL may enhance cardiovascular risk assessment and stratification (11).

 

Methods for Measuring Oxidative Status and Oxidative Stress

    1. MEASUREMENT OF ANTI-OXIDIZED LDL AUTOANTIBODIES (anti-oxLDL antibodies)

ELISA for the detection of Anti-oxidized LDL Autoantibodies (oLAB ) | BI-20032

• Sample type – serum
• Sample volume –  50µl/well
• Incubation time –  1.5 h / 30 min / 15 min
• Detection range – 0 – 1200 mU / ml
• Sensitivity – 48 mU / ml
• Precision-  In-between-run (n=5): ≤ 8 % CV, Within-run (n=8): ≤ 4 % CV
• Use – Research use only
• Widely cited in over 70 publications

Protocol booklet and MSDS

 

2. MEASUREMENT OF BIOLOGICAL PEROXIDES 

Oxidative Stress Test – OXYSTAT Assay | BI-5007

Quick and easy assay to measure total peroxides in biological fluids.

• Method – colorimetric assay, 96 wells
• Sample type – serum, plasma, biological fluids
• Sample volume – 10µl/well
• Assay time – 15 min
• Detection range – 0 – 660 µmol/l
• Sensitivity – 7 µmol/l
• Use – Research use only
• Widely cited in over 60 publications

 Protocol booklet and MSDS

Results indicate a direct relationship between free radicals and circulating biological peroxides, enabling the assessment of oxidative status in biological samples.

 

Literature

1. Cardiovascular diseases (CVDs). World Health Organization; 2025.
2. Free radicals and oxidative stress: Mechanisms and therapeutic targets. Hassan HA, Ahmed HS, Hassan DF. Hum Antibodies. 2024;32(4):151-167. doi: 10.3233/HAB-240011. PMID: 39031349.
3. Interplay of oxidative stress, cellular communication and signaling pathways in cancer. Iqbal MJ, Kabeer A, Abbas Z, Siddiqui HA, Calina D, Sharifi-Rad J, Cho WC. Cell Commun Signal. 2024 Jan 2;22(1):7. doi: 10.1186/s12964-023-01398-5. PMID: 38167159; PMCID: PMC10763046.
4. Oxidative Stress: Pathogenetic Role in Diabetes Mellitus and Its Complications and Therapeutic Approaches to Correction. Darenskaya MA, Kolesnikova LI, Kolesnikov SI. Bull Exp Biol Med. 2021 May;171(2):179-189. doi: 10.1007/s10517-021-05191-7. Epub 2021 Jun 26. PMID: 34173093; PMCID: PMC8233182.
5. Mechanisms of Oxidative Stress in Metabolic Syndrome. Masenga SK, Kabwe LS, Chakulya M, Kirabo A. Int J Mol Sci. 2023 Apr 26;24(9):7898. doi: 10.3390/ijms24097898. PMID: 37175603; PMCID: PMC10178199.
6. Oxidative stress: The core pathogenesis and mechanism of Alzheimer’s disease. Bai R, Guo J, Ye XY, Xie Y, Xie T. Ageing Res Rev. 2022 May;77:101619. doi: 10.1016/j.arr.2022.101619. Epub 2022 Apr 5. PMID: 35395415.
7. The Role of Oxidative Stress in Atherosclerosis. Batty M, Bennett MR, Yu E. Cells. 2022 Nov 30;11(23):3843. doi: 10.3390/cells11233843. PMID: 36497101; PMCID: PMC9735601.
8. Oxidative Stress in Cardiovascular Diseases. Dubois-Deruy E, Peugnet V, Turkieh A, Pinet F. Antioxidants (Basel). 2020 Sep 14;9(9):864. doi: 10.3390/antiox9090864. PMID: 32937950; PMCID: PMC7554855.
9. Pathophysiology of Atherosclerosis. Jebari-Benslaiman S, Galicia-García U, Larrea-Sebal A, Olaetxea JR, Alloza I, Vandenbroeck K, Benito-Vicente A, Martín C. Int J Mol Sci. 2022 Mar 20;23(6):3346. doi: 10.3390/ijms23063346. PMID: 35328769; PMCID: PMC8954705.
10. Oxidized LDL and anti-oxidized LDL antibodies in atherosclerosis – Novel insights and future directions in diagnosis and therapy. Hartley A, Haskard D, Khamis R. Trends Cardiovasc Med. 2019 Jan;29(1):22-26. doi: 10.1016/j.tcm.2018.05.010. Epub 2018 Jun 4. PMID: 29934015.

11. Overview of Clinical Relevance of Antibodies Against Oxidized Low-Density Lipoprotein (oLAb) Within Three Decades by ELISA Technology. Antioxidants (Basel). Wonisch W, Tatzber F, Lindschinger M, Falk A, Resch U, Mörkl S, Zarkovic N, Cvirn G 2024 Dec 19;13(12):1560. doi: 10.3390/antiox13121560. PMID: 39765889; PMCID: PMC11672888.

 

NT-proBNP at Dialysis Initiation-Predictor of Heart Disease Hospitalization: Patients with end-stage kidney disease (ESKD) face a cardiovascular (CV) death risk approximately 10 to 20 times higher than that of the general population. Cardiac biomarkers serve as a valuable tool to predict CV morbidity and mortality in asymptomatic individuals.

About NT-proBNP

N-terminal pro-BNP (NT-proBNP) is a biomarker released by the heart in response to ventricular stretch and stress. It is commonly used to diagnose and manage heart failure, as elevated levels indicate cardiac dysfunction. NT-proBNP levels can also provide prognostic information regarding cardiovascular risk and outcomes in various conditions, including coronary artery disease, sepsis, and in patients with end-stage kidney disease (1).

NT-proBNP at Dialysis Initiation-Predictor of Heart Disease Hospitalization

A study by Shimohata H. et al, investigated if NT-proBNP measurement at the initiation of dialysis therapy is useful to predict later hospitalization for ischemic heart disease (IHD). The results demonstrated that NT-proBNP measurement at the initiation of dialysis therapy is useful to predict later hospitalization for IHD .

NT-pro BNP level at dialysis initiation is a useful biomarker for predicting hospitalization for ischemic heart disease.

NT-proBNP was measured with the ELISA assay from BIOMEDICA

NT-proBNP ELISA assay kit (cat. no. SK-1204)

EASY – simple 2 step protocol, can be run in every lab
CONVENIENT – high and low kit controls included 
RELIABLE – validated according to international quality guidelines (see validation data )
TRUSTED – widely cited in 140 publications

 

Related Products:

Rat NT-proBNP ELISA (cat. no. BI-1204R)

BNP Fragment EIA (cat. no. 20852W)

 

Literature

1. NT-pro BNP level at dialysis initiation is a useful biomarker for predicting hospitalization for ischemic heart disease. Shimohata H, Usui J, Tawara-Iida T, Ebihara I, Ishizu T, Maeda Y, Kobayashi H, Numajiri D, Kaneshige A, Sega M, Yamashita M, Ohgi K, Maruyama H, Takayasu M, Hirayama K, Kobayashi M, Yamagata K; Study Group of the Ibaraki Dialysis Initiation Cohort Study. Clin Exp Nephrol. 2024 May;28(5):457-464. doi: 10.1007/s10157-023-02442-x.
2. Association of NT-proBNP and BNP With Future Clinical Outcomes in Patients With ESKD: A Systematic Review and Meta-analysis. Harrison TG, Shukalek CB, Hemmelgarn BR, Zarnke KB, Ronksley PE, Iragorri N, Graham MM, James MT. Am J Kidney Dis. 2020 Aug;76(2):233-247. doi: 10.1053/j.ajkd.2019.12.017. Epub 2020 May 6. PMID: 32387090.

 

Abstract

Background: Patients with end-stage kidney disease (ESKD) are at high risk of cardiovascular disease including stroke, heart failure, and ischemic heart disease (IHD). To prevent the occurrence and progression of CVD, a reliable prognostic cardiac biomarker is essential. We investigated the prognostic value of NT-proBNP for each incident type of CVD.

Methods: Male patients from the Ibaraki Dialysis Initiation Cohort (iDIC) study with preserved serum samples from dialysis initiation day (n = 212) were analyzed. Patients were classified into four groups according to quartiles of baseline NT-pro BNP levels. The relationship between NT-proBNP levels at the initiation of dialysis and the subsequent incidence of hospitalization events due to IHD, heart failure, and stroke was analyzed.

Results: The incidence rate for hospitalization due to IHD was significantly higher in the highest NT-proBNP category (Log rank p = 0.008); those of stroke and heart failure showed no significant differences among quartiles. Cox proportional hazards regression analysis revealed that serum NT-proBNT was the only prognostic factor for hospitalization for IHD after adjustment by major known IHD risk factors. (HR, 1.008; 95% confidence interval, 1.002-1.014; p = 0.01) The ROC curve analysis for the incidence of hospitalization due to IHD showed that NT-proBNP had an area under the curve (AUC) of 0.759 (95% CI 0.622-0.897; p = 0.004) at a cut-off value of 956.6 pg/mL.

Conclusion: NT-proBNP measurement at the initiation of dialysis therapy is useful to predict later hospitalization for IHD.

 

 

Big Endothelin-1 (Big ET-1) is the precursor to the most potent vasoconstrictor peptide Endothelin-1 (ET-1), which is mainly produced by endothelial cells (1). Interestingly, there is evidence of stimulated ET-1 release from various immune cells, including macrophages and dendritic cells, indicating that these cells can also synthesize ET-1 (2).

While ET-1 is essential in regulating vascular tone and blood pressure, Big ET-1 itself is biologically inactive and mainly functions as a reservoir for ET-1. Big ET-1 has a longer half-life compared to ET-1 and circulates in equal molar amounts, making it a more stable and reliable biomarker (3). Elevated levels of Big ET-1 can signal vascular dysfunction and are linked to cardiovascular conditions such as hypertension and heart failure (4).

Prognostic value of Big Endothelin-1 in heart failure

A study recently explored the prognostic value of Big ET-1 in 4,368 patients hospitalized with heart failure with a median follow-up of 875 days (5).

Key findings:

• Elevated Big ET-1 was independently associated with cardiovascular death in patients with HF.
• Big ET-1 is a promising indicator of HF prognosis.

 

Big Endothelin-1 and NT-proBNP were measured with the following ELISA assay kits:

Big Endothelin-1 ELISA | BI-20082H

• Direct measurement – 50µl serum/plasma per well.
• High Quality – fully validated according to international quality guidelines
• Trusted – cited in over 90 publications
• Protocol booklet click here

 

NT-proBNP ELISA | SK-1204

• Convenient – ready -to-use reagents
• Flexible – can be run in every lab
• Two controls included
• High quality – fully validated according to international quality guidelines
• Trusted- cited in over 140 publications
• Protocol booklet click here

 

 

Literature

1. Endothelin-1 in Health and Disease. Banecki KMRM, Dora KA. Int J Mol Sci. 2023 Jul 10;24(14):11295. doi: 10.3390/ijms241411295. PMID: 37511055; PMCID: PMC10379484.
2. Endothelin-1 in Health and Disease. Banecki KMRM, Dora KA. Int J Mol Sci. 2023 Jul 10;24(14):11295. doi: 10.3390/ijms241411295. PMID: 37511055; PMCID: PMC10379484.
3. Biomarkers in aortic dissection. Wen D, Zhou XL, Li JJ, Hui RT. Clin Chim Acta. 2011 Apr 11;412(9-10):688-95. doi: 10.1016/j.cca.2010.12.039. Epub 2011 Jan 13. PMID: 21237193.
4. Plasma concentration of big endothelin-1 and its relation with plasma NT-proBNP and ventricular function in heart failure patients. Rivera M, Cortés R, Portolés M, Valero R, Sancho-Tello MJ, Martínez-Dolz L, Sevilla B, Taléns-Visconti R, Jordán A, Miró V, Pérez-Boscá JL, Marín F, Climent V, García de Burgos F, Payá R, Sogorb F, Bertomeu V, Salvador A. Rev Esp Cardiol. 2005 Mar;58(3):278-84. Spanish. PMID: 15766450.
5. Prognostic Value of Plasma Big Endothelin-1 in Patients Hospitalized for Heart Failure. Wang J, Feng J, Tse G, Zhai M, Huang Y, Zhou Q, Zhuang X, Liu H, Zhang Y, Zhang J. Korean Circ J. 2025 Aug;55(8):705-717. doi: 10.4070/kcj.2024.0354. Epub 2025 Apr 11. PMID: 40345830; PMCID: PMC12314060.  

 

 

Prognostic Value of Plasma Big Endothelin-1 in Patients Hospitalized for Heart Failure.

Abstract:

Background and objectives: Endothelin-1 (ET-1) is a potent vasoconstrictor and multifunctional neuroendocrine hormone that is closely associated with the pathophysiology of heart failure (HF). Currently, the evidence about the predictive value of big ET-1 in HF remains insufficient. This study aims to investigate the prognostic importance of big ET-1 in HF.

Methods: We examined the incidence of cardiovascular death in a single-center retrospective cohort of HF (de novo, worsening, or chronic included).

Results: The 4,368 hospitalized HF patients were enrolled. During the median follow-up of 875 (365-1,400) days, 851 (19.5%) patients had primary outcome events. Big ET-1 was independently associated with cardiovascular death as a continuous variable (hazard ratio [HR], 1.13; 95% confidence interval [CI], 1.06-1.21; p<0.001) and by tertiles (HR, 1.35; 95% CI, 1.06-1.72; p=0.017 for tertile 2 and HR, 1.70; 95% CI, 1.32-2.19; p<0.001 for tertile 3). This pattern of risk was maintained after further adjustment for NT-proBNP (HR, 1.11; 95% CI, 1.03-1.19; p=0.006 for continuous variable, HR, 1.30; 95% CI, 1.02-1.67; p=0.035 for tertile 2, and HR, 1.69; 95% CI, 1.23-2.05; p=0.034 for tertile 3). Net reclassification index (NRI) and integrated discrimination improvement (IDI) analysis showed that big ET-1 provided additional predictive power in combination with NT-proBNP (NRI, 0.11; 95% CI, 0.04-0.17; p=0.012 and IDI, 0.012; 95% CI, 0.003-0.017; p<0.001).

Conclusions: Elevated big ET-1 was independently associated with cardiovascular death in patients with HF. Big ET-1 may be a promising indicator of HF prognosis. In combination with NT-proBNP, big ET-1 may provide incremental predictive information.

 

 

 

 

 

 

 

 

 

 

February is designated as “Heart Month,” a time to raise awareness about cardiovascular health, promoting healthy lifestyles, and encouraging prevention of heart disease. It aims to educate the public on the risk factors, symptoms, and treatments associated with heart-related conditions, highlighting the importance of maintaining a healthy heart through proper nutrition, regular exercise, avoiding smoking, managing stress, and monitoring blood pressure and cholesterol levels (1-3).

HEART MONTH – focusing on heart health and prevention

Biomarkers in cardiovascular disease

Biomarkers can serve as biochemical indicators that offer crucial insights into disease prognosis and progression, and in predicting the response to treatments. Biomarkers are also utilized in clinical trials or applied in toxicology, including preclinical drug safety evaluations. Advances in biomarker research have transformed how heart conditions are diagnosed and managed (4).

Biomedica offers a wide range of ELISA kits for the accurate measurement of biomarkers related to heart and cardiovascular diseases including NT-proBNP, Big Endothelin-1, FGF23, and markers related to oxidative stress.

• NT-proBNP – human (cat. no. SK-1204)
• NT-proBNP- rat  (cat. no. BI-1204R)
• NT-proANP – human, rodent (cat. no. BI-20892 )
• Big Endothelin-1 (cat. no. BI-20082H)
• FGF23 intact (cat. no. BI-20700)
• FGF23 c-terminal (cat. no. BI-20702)
• Endostatin
• Oxidized LDL (low density lipoprotein) antibodies, oLAB – (BI-20032)
• IL-6 (cat. no. BI-IL6)

 

NT-proBNP ∙ NT-proANP ∙ BigET-1 ∙ FGF23 ∙ Endostatin ∙ LRG1 ∙ oxLDL Antibodies ∙ IL-6

 

NT-proBNP (N-terminal pro b-type natriuretic peptide) is the inactive amino-terminal fragment cleaved from proBNP, a prohormone produced predominantly by ventricular myocytes in response to increased myocardial wall stress and volume overload. Due to its stability and longer half-life compared to active BNP, NT-proBNP serves as a sensitive and specific biomarker for the diagnosis of heart failure.  NT-proBNP is commonly used in the diagnosis and management of heart failure, reflecting increased intracardiac pressures and ventricular dilation (5-7). It aids in differentiating cardiac from non-cardiac causes of dyspnea, stratifying disease severity, guiding therapeutic decisions, and predicting morbidity and mortality outcomes in heart failure patients (8).

NT-proANP (N-terminal pro-atrial natriuretic peptide) is a biomarker released by the heart in response to atrial stretching and elevated blood volume. It is utilized to evaluate heart failure and detect cardiac stress, helping in the diagnosis and management of various cardiovascular conditions (9).

Big Endothelin-1 (Big ET-1) is a vasoconstrictive peptide and the precursor to Endothelin-1 (ET-1), which is the biologically active form. Elevated levels of Big ET-1 serve as an independent marker of heart failure in cases of congestive heart disease (10). Due to its longer half-life compared to ET-1 and its presence in circulation in equimolar amounts with ET-1, Big ET-1 is considered a more reliable biomarker.

Fibroblast Growth Factor-23 (FGF23) is a hormone involved in regulating phosphate metabolism. It has emerged as a potential biomarker for cardiovascular risk, with elevated circulating FGF23 levels being linked to adverse outcomes such as heart failure and arrhythmias (11, 12).

Endostatin, a fragment derived from collagen XVIII, is an extracellular matrix protein that plays a crucial role in the development of chronic kidney and heart diseases. In this study by Yaghoubi A et al, Endostatin levels were found to be elevated in patients hospitalized with acute dyspnea who had a history of chronic heart failure (CHF), and these elevated levels were associated with increased mortality at 3 months. Additionally, endostatin was linked to both 1-month and 3-month mortality in patients presenting with acute dyspnea who had no previous history of CHF (13, 14).

Leucine-rich alpha-2-glycoprotein (LRG) is a secreted protein that plays a significant role in pathological ocular neovascularization. It is also implicated in various conditions such as cardiovascular disease, diabetes, inflammatory disorders, and cancer. Recent research has identified LRG as an independent predictor of diastolic dysfunction (DD), due to myocardial fibrosis (15).

Oxidized LDL (low density lipoprotein) antibodies, oLAB 

Oxidized LDL (oxLDL) antibodies are directed against epitopes on oxidized low-density lipoprotein particles. OxLDL results from the oxidative modification of native LDL particles, involving lipid peroxidation and protein oxidation, which generate neoantigens recognized as foreign by the immune system (12). The production of anti-oxLDL antibodies, predominantly IgG and IgM subclasses, reflects ongoing oxidative stress and lipid peroxidation processes within atherosclerotic lesions. These antibodies can participate in immune complex formation, potentially influencing atherogenesis through pro-inflammatory or anti-inflammatory mechanisms. Elevated levels of anti-oxLDL antibodies have been correlated with the presence and progression of atherosclerotic plaques, making them valuable biomarkers for cardiovascular disease risk assessment. Their precise role in atherosclerosis pathophysiology remains complex, involving both protective clearance of modified lipoproteins and pro-inflammatory immune responses that may exacerbate vascular injury (16-18).

Interleukin-6 (IL-6)

IL-6 signaling plays a critical role in the inflammatory processes underlying cardiovascular disease (CVD). IL-6 is a cytokine that promotes inflammation, endothelial dysfunction, and plaque formation in atherosclerosis (15). It signals through its receptor complex, activating pathways such as JAK/STAT, which contribute to vascular inflammation and instability. Anti-IL-6 therapeutics, including monoclonal antibodies like tocilizumab, target this cytokine or its receptor to reduce inflammation. These agents have shown potential in lowering cardiovascular risk by modulating inflammatory responses, making IL-6 inhibition a promising strategy for managing CVD associated with chronic inflammation (19, 20).

 

Literature

1. 2021 Dietary Guidance to Improve Cardiovascular Health: A Scientific Statement From the American Heart Association. Lichtenstein AH, Appel LJ, Vadiveloo M, Hu FB, Kris-Etherton PM, Rebholz CM, Sacks FM, Thorndike AN, Van Horn L, Wylie-Rosett J. Circulation. 2021 Dec 7;144(23):e472-e487. doi: 10.1161/CIR.0000000000001031. Epub 2021 Nov 2. PMID: 34724806.
2. A Heart-Healthy Diet for Cardiovascular Disease Prevention: Where Are We Now? Diab A, Dastmalchi LN, Gulati M, Michos ED. Vasc Health Risk Manag. 2023 Apr 21;19:237-253. doi: 10.2147/VHRM.S379874. PMID: 37113563; PMCID: PMC10128075.
3. Physical Activity Over the Lifecourse and Cardiovascular Disease. Perry AS, Dooley EE, Master H, Spartano NL, Brittain EL, Pettee Gabriel K. Circ Res. 2023 Jun 9;132(12):1725-1740. doi: 10.1161/CIRCRESAHA.123.322121. Epub 2023 Jun 8. PMID: 37289900; PMCID: PMC10254078.
4. Advancements in Biomarkers for Early Detection and Risk Stratification of Cardiovascular Diseases-A Literature Review. Nazir A, Nazir A, Afzaal U, Aman S, Sadiq SUR, Akah OZ, Jamal MSW, Hassan SZ. Health Sci Rep. 2025 May 26;8(5):e70878. doi: 10.1002/hsr2.70878. PMID: 40432692; PMCID: PMC12106349.
5. Natriuretic Peptides: Role in the Diagnosis and Management of Heart Failure: A Scientific Statement From the Heart Failure Association of the European Society of Cardiology, Heart Failure Society of America and Japanese Heart Failure Society. Tsutsui H, Albert NM, Coats AJS, Anker SD, Bayes-Genis A, Butler J, Chioncel O, Defilippi CR, Drazner MH, Felker GM, Filippatos G, Fiuzat M, Ide T, Januzzi JL Jr, Kinugawa K, Kuwahara K, Matsue Y, Mentz RJ, Metra M, Pandey A, Rosano G, Saito Y, Sakata Y, Sato N, Seferovic PM, Teerlink J, Yamamoto K, Yoshimura MJ Card Fail. 2023 May;29(5):787-804. doi: 10.1016/j.cardfail.2023.02.009. Epub 2023 Apr 17. PMID: 37117140.
6. Practical algorithms for early diagnosis of heart failure and heart stress using NT-proBNP: A clinical consensus statement from the Heart Failure Association of the ESC. Bayes-Genis A, Docherty KF, Petrie MC, Januzzi JL, Mueller C, Anderson L, Bozkurt B, Butler J, Chioncel O, Cleland JGF, Christodorescu R, Del Prato S, Gustafsson F, Lam CSP, Moura B, Pop-Busui R, Seferovic P, Volterrani M, Vaduganathan M, Metra M, Rosano G. Eur J Heart Fail. 2023 Nov;25(11):1891-1898. doi: 10.1002/ejhf.3036. Epub 2023 Sep 26. PMID: 37712339.
7. Essential biochemistry and physiology of (NT-pro)BNP. Hall C.Eur J Heart Fail. 2004;6:257–260. doi:10.1016/j.ejheart.2003.12.015.
8. Comprehensive Review of Cardiovascular Disease Management: Cardiac Biomarkers, Imaging Modalities, Pharmacotherapy, Surgical Interventions, and Herbal Remedies. Netala VR, Teertam SK, Li H, Zhang Z. A Cells. 2024 Sep 1;13(17):1471. doi: 10.3390/cells13171471. PMID: 39273041; PMCID: PMC11394358.
9. Prognostic value of NT-proANP levels on major cardiovascular outcomes in a 31-year follow-up study depends on baseline morbidity. Sakko S, Perkiömäki J, Ylitalo A, Huikuri H, Ukkola O, Koivunen P, Tapio J. Sci Rep. 2025 May 28;15(1):18660. doi: 10.1038/s41598-025-03819-6. PMID: 40436983; PMCID: PMC12119872.
10. Elevated Plasma Big Endothelin-1 at Admission Is Associated With Poor Short-Term Outcomes in Patients With Acute Decompensated Heart Failure. Mo R, Yang YM, Yu LT, Tan HQ, Zhu J. Front Cardiovasc Med. 2021 Mar 11;8:629268. doi: 10.3389/fcvm.2021.629268. PMID: 33778022; PMCID: PMC7990871.
11. An Overview of FGF-23 as a Novel Candidate Biomarker of Cardiovascular Risk. Vázquez-Sánchez S, Poveda J, Navarro-García JA, González-Lafuente L, Rodríguez-Sánchez E, Ruilope LM, Ruiz-Hurtado G. Front Physiol. 2021 Mar 9;12:632260. doi: 10.3389/fphys.2021.632260. PMID: 33767635; PMCID: PMC7985069.
12. Discharge FGF23 level predicts one year outcome in patients admitted with acute heart failure. Vergaro G, Aimo A, Taurino E, Del Franco A, Fabiani I, Prontera C, Masotti S, Musetti V, Emdin M, Passino C. Int J Cardiol. 2021 Aug 1;336:98-104. doi: 10.1016/j.ijcard.2021.05.028. Epub 2021 May 19. PMID: 34019969.
13. Endostatin in Renal and Cardiovascular Diseases. Li M, Popovic Z, Chu C, Krämer BK, Hocher B. Kidney Dis (Basel). 2021 Sep 9;7(6):468-481. doi: 10.1159/000518221. PMID: 34901193; PMCID: PMC8613550.
14. Association between endostatin and mortality in patients with acute dyspnoea, with or without congestive heart failure: a single-centre, prospective, observational study. Yaghoubi A, Heijl C, Khoshnood AM, Wändell PE, Carlsson AC, Wessman T. BMJ Open. 2025 Jan 11;15(1):e085238. doi: 10.1136/bmjopen-2024-085238. PMID: 39800400; PMCID: PMC11752042.
15. Leucine-Rich Alpha-2-Glycoprotein: A Novel Predictor of Diastolic Dysfunction. Loch A, Tan KL, Danaee M, Idris I, Ng ML. Biomedicines. 2023 Mar 20;11(3):944. doi: 10.3390/biomedicines11030944. PMID: 36979923; PMCID: PMC10045934.
16. Immune response to lipoproteins in atherosclerosis. Samson S, Mundkur L, Kakkar VV. 2012;2012:571846. doi: 10.1155/2012/571846. Epub 2012 Aug 23. PMID: 22957222; PMCID: PMC3432325.
17. Antibodies against human oxidized low-density lipoprotein (LDL) as markers for human plasma modified lipoproteins. Radulescu L, Stancu C, Antohe F. Med Sci Monit. 2004 Jul;10(7):BR207-14. Epub 2004 Jun 29. PMID: 15232494.
18. Oxidized LDL and anti-oxidized LDL antibodies in atherosclerosis – Novel insights and future directions in diagnosis and therapy .Hartley A, Haskard D, Khamis R. Trends Cardiovasc Med. 2019 Jan;29(1):22-26. doi: 10.1016/j.tcm.2018.05.010. Epub 2018 Jun 4. PMID: 29934015.
19. IL-6 and Cardiovascular Risk: A Narrative Review. Mehta NN, deGoma E, Shapiro MD. Curr Atheroscler Rep. 2024 Nov 26;27(1):12. doi: 10.1007/s11883-024-01259-7. PMID: 39589436; PMCID: PMC11599326.
20. Interleukin-6 Signaling and Anti-Interleukin-6 Therapeutics in Cardiovascular Disease. Ridker PM, Rane M. Circ Res. 2021 May 28;128(11):1728-1746. doi: 10.1161/CIRCRESAHA.121.319077. Epub 2021 May 17. PMID: 33998272.

 

 

 

Effect of left atrial appendage closure on heart failure biomarker NT-proANP.

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, affecting about 1-2% of the general population. The incidence of AF increases with age and AF carries a five-fold increased risk of cardioembolic events, accounting for roughly 20% of all strokes. Strokes related to AF tend to be more severe, often resulting in worse neurological outcomes (1).  

The left atrial appendage (LAA) is a finger-shaped extension originating from the main body of the left atrium. In AF, thrombus formation often occurs within the LAA due to decreased contractile function and blood flow stasis. 90% of thrombi in nonvalvular AF patients and 57% in valvular AF patients are located in the left atrial appendage (LAA). Though oral anticoagulants serve as the primary treatment for preventing strokes in patients with atrial fibrillation, they are not suitable for all patients due to certain contraindications. Targeting the LAA has emerged as an alternative treatment approach to decrease the risk of stroke or systemic embolism in patients with atrial fibrillation (2-5).

In a study published in 2024, researchers investigated the impact of left atrial appendage (LAA) closure on systemic homeostasis in patients with atrial fibrillation. The study aimed to understand how occluding the LAA influences systemic biomarkers related to coagulation, inflammation, and endothelial function. Results suggest that LAA closure not only reduces stroke risk but may also favorably modulate systemic physiological processes, potentially contributing to improved overall cardiovascular health in these patients (5).

Effect of left atrial appendage closure on heart failure biomarker NT-proANP

In the subanalysis of this trial, researchers also examined the effects of left atrial appendage (LAA) closure on heart failure biomarkers, including NT-proBNP, NT-proANP, Galectin-3, and GDF-15 in patients with atrial fibrillation. The results demonstrated that LAA closure did not significantly influence the levels of HF biomarkers 6 months after the procedure. (6).

In a recent study researchers investigated the hemodynamic and echocardiography changes during and after LAA closure (7). Biomarkers for heart failure were measured including, N-terminal pro-B-type natriuretic peptide (NT-proBNP), N-terminal-pro-atrial natriuretic peptide (NT-proANP) and growth-differentiation factor-15 (GDF-15). The results show that LAA Closure was associated with an acute increase in both rest and postexercise LA pressure. The acute changes during LAAC were explained mostly by the saline and contrast dye given during LAAC and not by the worsening of the reservoir function associated with the procedure. In addition, no increase in NT-proANP and other HF biomarkers or changes in echocardiography parameters after 3 or 6 months after the procedure were observed (7).

About NT-proANP

NT-proANP (N-terminal pro-atrial natriuretic peptide) is a biomarker derived from the precursor of atrial natriuretic peptide (ANP), a hormone produced primarily by the atria of the heart. It plays a key role in regulating blood pressure, blood volume, and electrolyte balance by promoting natriuresis (excretion of sodium) and vasodilation.

Elevated levels of NT-proANP are often associated with conditions involving increased atrial pressure and volume overload, such as heart failure, atrial fibrillation, and other cardiac dysfunctions. Because it is relatively stable and easier to measure than active ANP, NT-proANP is frequently used in clinical settings to assess and monitor cardiac function.

About NT-proBNP

NT-proBNP (N-terminal pro-B-type natriuretic peptide) is a biomarker released from the heart in response to increased wall stress, typically due to conditions like heart failure. It is a non-active fragment of the prohormone BNP (B-type natriuretic peptide), which is produced mainly by the ventricles of the heart when they are under strain.

Elevated levels of NT-proBNP are indicative of cardiac stress and are commonly used in clinical practice to diagnose, assess the severity, and monitor the progression of heart failure. It also helps differentiate cardiac from non-cardiac causes of symptoms such as shortness of breath. Because NT-proBNP is stable in blood samples and has a longer half-life than BNP, it is a reliable biomarker for evaluating cardiac function across various clinical settings.

 

NT proANP ELISA (cat. No. BI-20892) Assay Kit

• CONVENIENT – small sample volume – 10 µl / well
• HIGH QUALITY kit – full validation package
• TRUSTED – cited in over 175 publications
• EASY – color coded and ready to use reagents
• FLEXIBLE- assay is suitable for human and non-human samples (rodents and others)

 

NT-proBNP (cat. no. SK-1204) ELISA Assay Kit

• TRUSTED – widely cited in over 140 publications 
• HIGH QUALITY kit – fully validated assays following international quality guidelines
• CONVENIENT – kits include pre-diluted calibrators and 2 controls

 

RAT NT-proBNP ELISA (BI-1204R) Assay Kit

• CONVENIENT – 10µl sample/well, kit control included
• TRUSTED – sample values provided

 

 

 Literature 

1. Left Atrial Appendage Closure and Systemic Homeostasis: The LAA HOMEOSTASIS Study. Lakkireddy D, Turagam M, Afzal MR, Rajasingh J, Atkins D, Dawn B, Di Biase L, Bartus K, Kar S, Natale A, Holmes DJ Jr.J Am Coll Cardiol. 2018 Jan 16;71(2):135-144. doi: 10.1016/j.jacc.2017.10.092. Erratum in: J Am Coll Cardiol. 2018 Feb 6;71(5):590. doi: 10.1016/j.jacc.2018.01.005. PMID: 29325636.
2. The Left Atrial Appendage: Target for Stroke Reduction in Atrial Fibrillation. Ramlawi B, Abu Saleh WK, Edgerton J. Methodist Debakey Cardiovasc J. 2015 Apr-Jun;11(2):100-3. doi: 10.14797/mdcj-11-2-100. PMID: 26306127; PMCID: PMC4547664.
3. The left atrial appendage: anatomy, function, and noninvasive evaluation. Beigel R, Wunderlich NC, Ho SY, Arsanjani R, Siegel RJ. JACC Cardiovasc Imaging. 2014 Dec;7(12):1251-65. doi: 10.1016/j.jcmg.2014.08.009. PMID: 25496544.
4. Left atrial appendage exclusion in atrial fibrillation. Rozen G, Margolis G, Marai I, Roguin A, Rahamim E, Planer D, Heist EK, Amir O, Tahiroglu I, Ruskin J, Mansour M, Elbaz-Greener G. Front Cardiovasc Med. 2022 Sep 13;9:949732. doi: 10.3389/fcvm.2022.949732. PMID: 36176999; PMCID: PMC9513198.
5. Left atrial appendage closure for stroke prevention in atrial fibrillation: current status and perspectives. Landmesser U, Skurk C, Tzikas A, Falk V, Reddy VY, Windecker S. Eur Heart J. 2024 Aug 21;45(32):2914-2932. doi: 10.1093/eurheartj/ehae398. PMID: 39027946; PMCID: PMC11335376.
6. The effect of left atrial appendage closure on heart failure biomarkers: A PRAGUE-17 trial subanalysis. Herman D, Osmancik P, Neuzil P, Hala P, Lekesova V, Benesova K, Hozman M, Jarkovsky J, Novackova M, Widimsky P, Reddy VY; PRAGUE-17 Trial Investigators. J Cardiovasc Electrophysiol. 2021 Oct;32(10):2645-2654. doi: 10.1111/jce.15206. Epub 2021 Aug 26. PMID: 34402135.
7. Acute and Short‐Term Hemodynamic and Echocardiography Changes During and After Left Atrial Appendage Closure. Dalibor Herman, Petr Peichl, Marek Hozman, Bronislav Janek, Tomas Knize, Teodora Vichova, Hana Linkova, Jana Vesela, Jakub Karch, Naďa Valosková, Eva Borisincova, Pavel Osmancik, J Interventional Cardiology, Dec. 2025. https://doi.org/10.1155/joic/5515180Digital Object Identifier (DOI)

Children and adolescents with type 1 diabetes (T1D) frequently encounter issues related to bone health. Research consistently shows that young individuals with T1D have lower bone mineral density (BMD) than their healthy counterparts. Moreover, children with T1D exhibit compromised bone microarchitecture and decreased bone turnover. Together, these factors heighten the risk of fractures throughout their lifetime (1). In addition, advanced imaging techniques have revealed that the negative impact of T1D on the growing skeleton goes beyond reduced bone density, affecting bone size, shape, and strength (2).

Type 1 diabetes in adolescents linked to low bone mass and altered bone biomarkers

In a recent study, researchers investigated whether adolescents with well-controlled, long-duration type 1 diabetes (T1D) have differences in bone mass and bone biomarkers in comparison with healthy individuals (3). The researchers measured various biomarkers including receptor activator nuclear factor κB ligand (RANKL*), Osteoprotegerin (OPG*), Sclerostin (SOST*), and C-terminal telopeptide of type I collagen (CTX).

Highlights

• Type 1 diabetes (T1D) is linked to a higher risk of fractures.
• Prolonged T1D leads to low bone mass and impaired microarchitecture.
• The T1D group showed decreased levels of RANKL and CTX.

 

In summary: young people with long-term T1D show decreased gain in bone mass, impaired microarchitecture, and suppressed RANKL-driven osteoclast formation, leading to decreased bone resorption. Monitoring bone health is recommended for adolescents with T1D.

*Biomedica ELISA kits were used in this study.

BIOMEDICA´s ELISA kit highlights:
• Widely cited in clinical studies
• Reliable – validated according to international guidelines
• High sensitivity – measurable concentrations in healthy subjects
• HIGH quality guaranteed 

FREE soluble RANKL HS ELISA | BI-20462

•  High sensitivity – measurable concentrations in healthy subjects
• Only ELISA that measures free, uncomplexed soluble RANKL

 

 

Literature

1. Bone Health in Children and Adolescents with Type 1 Diabetes: Optimizing Bone Accrual and Preventing Fractures. Levran N, Shalev-Goldman E, Levy-Shraga Y. Nutrients. 2025 Jul 23;17(15):2400. doi: 10.3390/nu17152400. PMID: 40805986; PMCID: PMC12348532.
2. Bone accrual in children and adolescents with type 1 diabetes: current knowledge and future directions. Weber DR Curr Opin Endocrinol Diabetes Obes. 2021 Aug 1;28(4):340-347. doi: 10.1097/MED.0000000000000638. PMID: 33965967.
3. Adolescents with long-duration type 1 diabetes have low bone mass and reduced levels of bone indices reflecting altered bone resorption. Swolin-Eide D, Pundziute Lyckå A, Novak D, Andersson B, Forsander G, Magnusson P.Bone. 2025 Oct;199:117560. doi: 10.1016/j.bone.2025.117560. Epub 2025 Jun 4. PMID: 40480641.

Intense exercise and load carriage can lead to high mechanical and metabolic stress on the skeleton, disrupting calcium metabolism (1). Studies have shown that load carriage exercise increases calcium absorption and retention in healthy young women (2). Integrating women into military service necessitates research on gender-specific effects of military training and operational activities (3). In a randomized controlled crossover trial researchers investigated the effect of calcium supplementation on calcium and bone metabolism in women during load carriage (1).  

The effect of calcium supplementation on bone calcium balance and calcium and bone metabolism during load carriage in women: a randomized controlled crossover trial. Coombs CV et al., 2025.

Study details:

• a total of 48 women volunteered for the study, including 38 military personnel and 10 civilians.
• each participant completed two load carriage exercise sessions in a randomized order:

•  One session after taking a 1000 mg calcium supplement, 60 minutes prior to load carriage
•  One session without any supplement (control)

• during each session, participants walked 12.8 km on a treadmill at a speed of 6.4 km/h for 120 minutes while carrying a 20 kg rucksack.

Calcium supplementation and bone health in woman during load carriage

Key findings:

• Intense exercise stresses the skeleton and disrupts calcium metabolism.
• Calcium supplementation leads to increased serum ionized calcium, reduced PTH levels, and decreased bone resorption.
• Calcium supplementation had no effect on markers of bone formation, including Sclerostin.
• Taking 1000 mg of calcium 60 minutes before load carriage helps protect bone health and calcium balance.

 

SCLEROSTIN was measured with the BIOMEDICA Sclerostin assay:

Sclerostin (SOST) ELISA  (cat. no. BI-20492)

• Most referenced Sclerostin ELISA in over 330 citations
• Low sample volume – 20µl / well
• Full validation package – download here

 

 

Related products:

Bioactive Sclerostin ELISA (cat. no. BI-20472)

OPG – Osteoprotegerin ELISA (cat. no. BI-20403)

FREE soluble RANKL HS ELISA (cat. no BI-20462)

 

Literature:

1. The effect of calcium supplementation on bone calcium balance and calcium and bone metabolism during load carriage in women: a randomized controlled crossover trial. Coombs CV, Greeves JP, Young CD, Irving AS, Eisenhauer A, Kolevica A, Heuser A, Tang JCY, Fraser WD, O’Leary TJ. J Bone Miner Res. 2025 Jun 3;40(6):753-765. doi: 10.1093/jbmr/zjaf004. PMID: 39804018.
2. Load carriage exercise increases calcium absorption and retention in healthy young women. Gaffney-Stomberg E, Nakayama AT, Lutz LJ, McClung JP, O’Brien KO, Staab JS. J Bone Miner Res. 2024 Mar 4;39(1):39-49. doi: 10.1093/jbmr/zjad003. PMID: 38630876.
3. Load carriage changes tibiofemoral arthrokinematics during ambulatory tasks in recruit-aged women. Johnson CC, Dzewaltowski AC, Dever DE, Krajewski KT, Rai A, Ahamed NU, Allison KF, Flanagan SD, Graham SM, Lovalekar M, Anderst WJ, Connaboy C. Sci Rep. 2024 Apr 25;14(1):9542. doi: 10.1038/s41598-024-60187-3. PMID: 38664550; PMCID: PMC11045865.

 

 

 

Fibroblast growth factor 23 (FGF23) plays a key role in mineral and bone disorders related to chronic kidney disease (CKD). Elevated FGF23 levels are linked to a higher risk of anemia in non-hemodialysis CKD and in patients undergoing hemodialysis. Researchers have identified a strong relationship between FGF23 and erythropoietin (EPO) resistance in hemodialysis (HD) patients. FGF23 is now recognized not only as a regulator of mineral metabolism but also as a direct inhibitor of erythropoiesis and a contributor to resistance against erythropoiesis-stimulating agents (ESAs) (1-3). 

Background:

-Erythropoietin (EPO) is a hormone produced mainly by the kidneys that regulates the production of red blood cells in the bone marrow, helping to maintain proper oxygen levels in the blood.

-Erythropoiesis-stimulating agents (ESAs) are medications that mimic the action of erythropoietin to stimulate the production of red blood cells in the bone marrow. They are commonly used to treat anemia, especially in patients with chronic kidney disease.

-High Fibroblast growth factor 23 (FGF23) levels are common in hemodialysis patients, mainly due to phosphate buildup from reduced kidney function.

 

FGF23 and EPO resistance in hemodialysis patients

A recent study by Hamano N. et al., explores the complex relationship between Fibroblast Growth Factor 23 (FGF23), endogenous erythropoietin (EPO), and the response to erythropoiesis-stimulating agents (ESAs) in hemodialysis patients. The research highlights how elevated FGF23 levels may influence erythropoietin production and resistance, impacting anemia management in chronic kidney disease (4).

FGF23 was measured in a cohort of 654 maintenance hemodialysis patients using the FGF23 ELISA assays from Biomedica.

FGF23 (C-terminal), cat. no. BI-20702 and FGF23 intact ELISA, cat. no. BI-20700 

• RELIABLE – validated following international quality guidelines
• CITED in over 80 publications
• EASY – 8 standards and 2 controls included
• For SERUM & PLASMA samples

 

Key findings:

-Elevated levels of FGF23 are associated with reduced natural EPO production.

-Higher ESA dose was associated with higher FGF23 levels measured by both intact and C-terminal assays.

-High FGF23 levels may contribute to erythropoietin resistance, making anemia harder to treat.

-Insights from the study may lead to new strategies to manage ESA resistance and enhance patient outcomes.

 

Fibroblast Growth Factor 23, Endogenous Erythropoietin, Erythropoiesis-Stimulating Agents, and Erythropoietin Resistance in Hemodialysis Patients. Hamano N et al., Am J Nephrol. 2025.

Abstract

Introduction: Recent experimental studies have reported that fibroblast growth factor 23 (FGF23) inhibits erythropoiesis by suppressing erythropoietin (EPO) production and downregulating the EPO receptor. Conversely, either endogenous or exogenous EPO has been shown to stimulate FGF23 production. However, little is known about the relationships between FGF23, erythropoiesis-stimulating agent (ESA) treatment, ESA resistance, and endogenous EPO in hemodialysis patients.

Methods: We analyzed cross-sectional data from a cohort of 654 maintenance hemodialysis patients. We examined the associations of intact or C-terminal FGF23 with ESA treatment, ESA resistance index (ERI), hemoglobin, C-reactive protein, and endogenous EPO levels using linear regression models. EPO was measured only in patients not receiving ESAs.

Results: A total of 458 patients (70%) were treated with ESAs. The median EPO concentration in non-ESA users was 7.8 (interquartile range, 5.3-14.4) mIU/mL. The median levels of intact and C-terminal FGF23 were 1,598 (interquartile range, 548-4,586) pg/mL and 38.7 (interquartile range, 14.0-127.6) pmol/L, respectively, in non-ESA users and 1,955 (interquartile range, 573-5,264) pg/mL and 41.4 (interquartile range, 13.9-116.8) pmol/L, respectively, in ESA users. After adjustment for potential confounders, higher ESA dose was associated with higher FGF23 levels measured by both intact and C-terminal assays. Higher C-terminal FGF23 was also associated with higher ERI, lower hemoglobin, and higher endogenous EPO, but no such associations were observed for intact FGF23 levels.

Conclusions: Both intact and C-terminal FGF23 showed similar associations with ESA dose, but they showed different patterns of association with other parameters related to anemia. Further research is needed to elucidate the mechanisms underlying these different associations.

 

 

 

Literature

1. Association of erythropoietin resistance and fibroblast growth factor 23 in dialysis patients: Results from the Japanese Dialysis Outcomes and Practice Patterns Study. Usui T, Zhao J, Fuller DS, Hanafusa N, Hasegawa T, Fujino H, Nomura T, Zee J, Young E, Robinson BM, Nangaku M.Nephrology (Carlton). 2021 Jan;26(1):46-53. doi: 10.1111/nep.13765. Epub 2020 Aug 20. PMID: 32743932; PMCID: PMC7754421.
2. Anemia and fibroblast growth factor 23 elevation in chronic kidney disease: homeostatic interactions and emerging therapeutics. Agoro R, White KE.Curr Opin Nephrol Hypertens. 2022 Jul 1;31(4):320-325. doi: 10.1097/MNH.0000000000000797. Epub 2022 Jun 10. PMID: 35703246; PMCID: PMC9307122.
3. The Role of Iron and Erythropoietin in the Association of Fibroblast Growth Factor 23 with Anemia in Chronic Kidney Disease in Humans. Bielesz B, Reiter T, Hammerle FP, Winnicki W, Bojic M, Gleiss A, Kieweg H, Ratzinger F, Sunder-Plassmann G, Marculescu R. J Clin Med. 2020 Aug 14;9(8):2640. doi: 10.3390/jcm9082640. PMID: 32823844; PMCID: PMC7463779.
4. Fibroblast Growth Factor 23, Endogenous Erythropoietin, Erythropoiesis-Stimulating Agents, and Erythropoietin Resistance in Hemodialysis Patients. Hamano N, Komaba H, Tanaka H, Takahashi H, Takahashi Y, Hyodo T, Hida M, Suga T, Wada T, Kakuta T, Fukagawa M, Komaba H. Am J Nephrol. 2025;56(4):403-411. doi: 10.1159/000543506. Epub 2025 Feb 20. PMID: 39978330.

 

 

Thirty-Year Outcomes of Immunosuppression Modulation

Over the past six decades, organ transplantation, especially pediatric liver transplantation, has revolutionized medical care by offering life-saving treatment options for children with end-stage liver disease (1). In a recent study, researchers investigated on how immunosuppressive therapy affects liver transplant outcomes in children during a thirty-year follow-up (2). Although pediatric liver transplantation is a life-saving procedure, it presents ongoing long-term challenges associated with immunosuppression (IS). Patients were classified according to their immunosuppression status at the final follow-up into three groups.

Pediatric Liver Transplantation

Thirty-Year Outcomes of Immunosuppression Modulation

Key Findings:
• The favorable histology and antibody profile observed in the IS-free group suggest the potential for sustained immune tolerance.
• Ongoing fibrosis in the IS-resumption group underscores the limitations of traditional immunosuppression strategies.
• Regular histological assessments and antibody monitoring may be beneficial for long-term immunosuppression management in pediatric liver transplant patients.

 

C4d a biomarker of transplant rejection

BIOMEDICA´s Anti-C4d Antibody Features – for the identification of human complement split product C4d in paraffin and frozen sections as well as by flow cytometry.

 

 Anti-C4d Antibody | BI-RC4D

• TRUSTED – widely cited in over 100 citations
• MULTI-USE – for immunohistochemistry on paraffin embedded tissue and frozen sections
• The C4d antibody has been utilized in kidney, heart, liver and other transplants
• working protocol

 

Anti-C4d Antibody (FITC) | BI-RC4D-FITC

• Protocol for cell- or solid-phase bound C4 and C4d split product by flow cytometry
• working protocol

 

-Explore our anti-C4d antibodies for IHC and FITC.

 

 

 

 

 

 

Our EZ4U Cell Proliferation and Cytotoxicity Assay was successfully applied in a recent study investigating novel therapeutic options for Cutaneous T-cell lymphoma (CTCL), a type of skin cancer that can also affect the blood (1). Extracorporeal photopheresis (ECP) is an immunomodulating photochemotherapy that has been linked to improved overall survival in the treatment of CTCL (2, 3).

MEASURING CELL VIABILITY with EZ4U Cell Proliferation and Cytotoxicity Assay

EZ4U Cell Proliferation & Cytotoxicity Assay (cat. no. BI-5000) – Assay Highlights

• Non-Radioactive & Non-Toxic
• Reliable & Sensitive
• Convenient single-step incubation for use on living cells
• Widely cited in over 290 publications !

 

Explore our product EZ4U Brochure link

 

Evidence of immunogenic cell death (ICD) and ICD-dependent dendritic cell activation induced by extracorporeal photopheresis in patients with leukaemic forms of cutaneous T-cell lymphoma. Lackner Aet al., Br J Dermatol. 2025.  

Abstract

Background: Despite novel therapeutic options, the long-term management of cutaneous T-cell lymphoma (CTCL) remains challenging. Extracorporeal photopheresis (ECP) is an immunomodulating photochemotherapy associated with higher overall survival when used for the treatment of leukaemic forms of CTCL. Its exact mode of action has not been fully elucidated. Immunogenic cell death (ICD) is pivotal in cancer immunotherapy, marked by the release of damage-associated molecular patterns that enhance dendritic cell (DC) maturation and cytotoxic T-lymphocyte responses.

Objectives: To explore ICD in patients with leukaemic forms of CTCL during ECP and its effect on DC activation.

Methods: We conducted in vitro studies with peripheral blood mononuclear cells (PBMCs) from healthy donors and ex vivo experiments with white blood cells (WBCs) from patients with leukaemic forms of CTCL undergoing ECP. We assessed cell viability, apoptosis and ICD markers [ATP, high mobility group box 1 protein (HMGB1), calreticulin] using flow cytometry, enzyme-linked immunosorbent assay and quantitative polymerase chain reaction. Engulfment assays evaluated DC activation by ECP-treated CD4+ T cells.

Results: ECP-treated healthy PBMCs and WBCs from patients with leukaemic forms of CTCL showed a significant induction of ICD hallmarks, including ATP release, HMGB1 secretion and calreticulin surface exposure. In patients with leukaemic forms of CTCL, calreticulin exposure was mainly present in CD4+CD26- T cells, indicating greater ICD susceptibility of malignant T cells. ECP-treated CD4+ T cells were phagocytosed by DCs, a process that was found to be dependent on ICD signals.

Conclusions: ECP induces ICD in malignant T cells and, to a lesser extent, in healthy T cells, facilitates DC activation. These findings suggest that ECP enhances targeted immune responses against malignant T cells in leukaemic forms of CTCL, offering new insights into its therapeutic mechanisms and potential applications in cancer immunotherapy.

 

Literature

1. Evidence of immunogenic cell death (ICD) and ICD-dependent dendritic cell activation induced by extracorporeal photopheresis in patients with leukaemic forms of cutaneous T-cell lymphoma. Lackner A, Burner T, Huber M, Dey S, Aigner S, Buxhofer-Ausch V, Geroldinger-Simic M, Iselin C, Chang YT, Tsai YC, Altrichter S, Wolf P, Kimeswenger S, Guenova E, Hoetzenecker W. Br J Dermatol. 2025 Jul 17;193(2):276-286. doi: 10.1093/bjd/ljaf102. PMID: 40112181.
2. Early intervention of extracorporeal photopheresis for advancing/progressing cutaneous T-cell lymphoma. Aires D, Abhyankar S.Hematol Oncol. 2023 Dec;41(5):809-816. doi: 10.1002/hon.3229. Epub 2023 Nov 16. PMID: 37974524.
3. Extracorporeal Photopheresis-An Overview. Front Med (Lausanne). Cho A, Jantschitsch C, Knobler R. 2018 Aug 27;5:236. doi: 10.3389/fmed.2018.00236. PMID: 30211164; PMCID: PMC6119964.

Nearly 10% of the world’s population suffer from lower back pain (LBP) (1, 2). Lumbar traction therapy is a non-invasive treatment for LBP that involves gently stretching the spine to relieve pressure on the vertebral discs and nerves (3). In a first-time study, researchers investigated the influence of long-term application of traction forces on the size of vertebrae, bone mineral density (BMD), and bone turnover markers in women LBP (4).

Impact of traction therapy on bone in women with chronic back pain

The BIOMEDICA free soluble RANKL (sRANKL) ELISA assay and bioactive Sclerostin ELISA assay were utilized in the study to quantify soluble RANKL and bioactive Sclerostin levels in human serum.

Soluble RANKL HS ELISA assay kit (cat. no. BI-20462)

• Highly sensitive – measurable concentrations in healthy individuals
• Only ELISA that measures free, uncomplexed soluble RANKL
• Widely cited in more than 325 publications

 

Bioactive SCLEROSTIN ELISA assay kit (cat.no. BI-20472) 

• Reliable – validated according to international guidelines
• Specific – high quality antibodies targeting the receptor binding region
• Low sample volume – 20 µl of serum/plasma per well 
• Citations

 

Bone remodelling after application of traction forces to the lumbar spine in women with chronic low back pain. Ratajczak M, Kusy K, Skrypnik D, Waszak M, Krutki P. Bone Joint Res. 2025 Aug 4;14(8):674-684. doi: 10.1302/2046-3758.148.BJR-2024-0465.R1. PMID: 40754314; PMCID: PMC12318618.

Abstract

Aims: The aim of the study was to investigate the effect of systematic lumbar traction, applied in 20 sessions over four weeks, on the size of vertebrae, bone mineral density (BMD), and bone turnover markers in women with chronic low back pain (LBP).

Methods: A total of 30 women with low back pain underwent 20 sessions of lumbar traction with a load of 25% to 30% of their body weight. Total body and lumbar spine BMD was measured using dual-energy X-ray absorptiometry, and bone turnover markers were determined using enzyme-linked immunosorbent assay (ELISA) with serum samples collected before the first traction session and 72 hours after the last traction session.

Results: After traction, decreased BMD and T-scores, a decreased mean vertebra width, and an increased mean height of L1-L4 segments were observed. The concentration of cross-linked C-telopeptide of type I collagen (CTXI) increased, while the concentration of receptor activator for nuclear factor κ B ligand (RANKL) decreased significantly after four weeks of traction. Sclerostin and procollagen 1 N-terminal propeptide (P1NP) concentrations remained unchanged.

Conclusion: Our study is the first to show the influence of traction forces on BMD and markers of bone metabolism. Future research with a longer follow-up period after traction is needed to better explore the direction of change.

 

Literature

1. The global epidemic of low back pain. Lancet Rheumatol. 2023 Jun;5(6):e305. doi: 10.1016/S2665-9913(23)00133-9. PMID: 38251593.
2. Low back pain, WHO, 2023.
3. What Is Traction Therapy, and How Does it Work? ERA Health.
4. Bone remodelling after application of traction forces to the lumbar spine in women with chronic low back pain. Ratajczak M, Kusy K, Skrypnik D, Waszak M, Krutki P. Bone Joint Res. 2025 Aug 4;14(8):674-684. doi: 10.1302/2046-3758.148.BJR-2024-0465.R1. PMID: 40754314; PMCID: PMC12318

Type 1 diabetes mellitus is an autoimmune disorder marked by the destruction of pancreatic islet cells, resulting in an absolute deficiency of insulin. Multiple mechanisms have been recognized to explain the skeletal fragility observed in T1DM, including reductions in bone mineral density (BMD), alterations in bone geometry, impaired bone microarchitecture, and compromised biomechanical properties, as evidenced in both humans and animal models of T1DM. Previous meta-analyses have shown that individuals with T1DM face a four- to sevenfold higher risk of hip fractures compared to controls (1, 2).

How Type 1 Diabetes affects Bone Health

In a recent cross-sectional clinical study researchers explored the differences in bone turnover markers (BTMs) and their correlations with areal mineral density (aBMD) in people with type 1 diabetes (T1D), to gain deeper insights into the mechanisms of skeletal fragility, including differences related to sex and hormonal factors (3).

Both the Biomedica BIOACTIVE SCLEROSTIN ELISA Assay and the FGF23 INTACT ELISA Assay were featured in this study.  

Bioactive Sclerostin ELISA (cat. no. BI-20472)

• Characterized antibodies that target the Sclerostin receptor binding region
• The assay is  validated for clinical samples  (validation data file)
• Only  20µl sample /well (protocol booklet)
• Widely cited

 

 FGF23 intact ELISA (cat. no. BI-20700)

• Extensively validated according to international quality guidelines
• Correlates with existing methods (validation data file)
• One-step ELISA  (protocol booklet)
• Cited in top-tier journals

 

Bone turnover markers and mineral density in type 1 diabetes – A cross-sectional study: DIAFALL. Rasmussen NH et al., Bone. 2025.

Abstract

Introduction/aim: This study investigated differences in bone turnover markers (BTMs) and their associations with areal bone mineral density (aBMD) in people with type 1 diabetes (T1D) to better understand the mechanisms underlying skeletal fragility, including sex- and hormone-related variations.

Methods: A cohort of 110 Caucasian participants with T1D were matched 1: 1 with age- and sex-matched controls. aBMD at the lumbar spine, femoral neck, legs, and arms was assessed using DXA. BTMs included P1NP, osteocalcin (OC), sclerostin, CTX-1, TRAcP, IGF-1, BASP, and osteopontin (OPN). Group comparisons were conducted using t-tests, and associations between BTMs and aBMD were examined using regression and Spearman correlations. Exploratory subgroup analyses stratified women by menopausal status.

Results: Bone formation markers (P1NP, OC) were significantly lower in T1D men compared to controls (P1NP: p = 0.046; OC: p = 0.002), reflecting suppressed bone formation. IGF-1 was reduced in both sexes (p < 0.001) and correlated positively with aBMD in women (p < 0.05), but not in men. Sclerostin levels were elevated in both sexes (p = 0.002-<0.001) without correlating with aBMD. CTX-1 was reduced in T1D men (p = 0.004), while TRAcP was elevated in both sexes (p = 0.044), correlating negatively with aBMD in women. Men with T1D had significantly lower leg aBMD (p = 0.032) and reduced femoral neck bone mineral content (p = 0.041). No overall differences were observed among women; however, exploratory analyses revealed that postmenopausal women with T1D had higher TRAcP and sclerostin levels and lower femoral neck aBMD compared to premenopausal counterparts.

Conclusion: T1D was associated with significant alterations in certain BTMs and reduced aBMD in men, while skeletal effects in women appeared to be influenced by menopausal status. The weak and mostly non-significant correlations between BTMs and aBMD suggest that impaired bone quality, rather than bone mass alone, may be the primary driver of skeletal fragility in T1D. Hormonal status may further modify these effects in women.

 

Literature

1. Fracture risk in young and middle-aged adults with type 1 diabetes mellitus: A systematic review and meta-analysis. Thong EP, Herath M, Weber DR, Ranasinha S, Ebeling PR, Milat F, Teede H. Clin Endocrinol (Oxf). 2018 Sep;89(3):314-323. doi: 10.1111/cen.13761. Epub 2018 Jul 3. PMID: 29876960; PMCID: PMC6105385.
2. Bone fragility in diabetes: novel concepts and clinical implications. Hofbauer LC, Busse B, Eastell R, Ferrari S, Frost M, Müller R, Burden AM, Rivadeneira F, Napoli N, Rauner M. Lancet Diabetes Endocrinol. 2022 Mar;10(3):207-220. doi: 10.1016/S2213-8587(21)00347-8. Epub 2022 Jan 31. PMID: 35101185.
3. Bone turnover markers and mineral density in type 1 diabetes – A cross-sectional study: DIAFALL. Rasmussen NH, Kvist AV, Lykkeboe S, Starup-Linde J, Handberg A, van den Bergh JP, Vestergaard P. Bone. 2025

Chronic inflammation is linked to various health disorders (1). Omega-6 polyunsaturated fatty acids (n-6 PUFAs), especially linoleic and arachidonic acid, have both pro- and anti-inflammatory effects, resulting in conflicting opinions on whether their consumption should be reduced (1, 2).

Omega-6 Fatty Acids and Biomarkers of Inflammation

In a recent study researchers explored whether red blood cell omega-6 polyunsaturated fatty acids (RBC n-6 PUFAs) are pro-inflammatory by examining their association with various inflammation biomarkers (4).

Red Blood Cell Omega-6 Fatty Acids and Biomarkers of Inflammation in the Framingham Offspring Study. Lai HTM et al., Nutrients. 2025.  

Abstract

Background/objectives: Chronic inflammation is recognized as an important risk factor for a variety of health disorders. Omega-6 polyunsaturated fatty acids (n-6 PUFAs), particularly linoleic (LA) and arachidonic acid (AA), have been shown to be either pro- or anti-inflammatory, and researchers have advocated both for and against reducing their dietary intake. This study sought to correlate the levels of ten inflammation-related biomarkers across multiple pathways with red blood cell (RBC) membrane levels of the major dietary and circulating n-6 PUFAs.

Methods: We included 2777 participants (mean age: 66 ± 9 years, 54% women, 9.8% minorities) from the Framingham Offspring and minority-enriched Omni cohorts, and calculated partial correlation coefficients.

Results: After multivariable adjustment, RBC LA was inversely correlated (all p ≤ 0.05) with five markers of inflammation, receptors, or pathways: C-reactive protein (r = -0.06); soluble interleukin-6 (r = -0.15); intercellular adhesion molecule-1 (r = -0.09); monocyte chemoattractant protein-1 (r = -0.07); and P-selectin (r = -0.07). RBC AA was inversely correlated (all p ≤ 0.05) with soluble interleukin-6 (r = -0.10); intercellular adhesion molecule-1 (r = -0.14); monocyte chemoattractant protein-1, and (r = -0.06); and osteoprotegerin (r = -0.07). Lipoprotein-associated phospholipase-A2 mass and activity, urinary isoprostanes, and tumor necrosis factor receptor-2 were not significantly correlated with LA or AA.

Conclusions: In our large community-based study, we observed weak but statistically significant inverse associations between several types of inflammatory biomarkers with RBC n-6 PUFAs. Our findings do not support the hypothesis that omega-6 fatty acids are pro-inflammatory.

 

The Biomedica Osteoprotegerin (OPG) ELISA assay was utilized in the above study.

Biomedica OPG ELISA (cat. no. BI-20403)

• RELIABLE – full validation protocol (spike recovery, dilution linearity. )
• EFFICIENT: only 20 µl sample / well (protocol booklet)
• TRUSTED – most referenced OPG ELISA, cited in over 270 publications

 

 

OPG ELISA Assay Principle:

 

Literature

1. Inflammation: The Cause of All Diseases. Chavda VP, Feehan J, Apostolopoulos V. 2024 Nov 18;13(22):1906. doi: 10.3390/cells13221906. PMID: 39594654; PMCID: PMC11592557.
2. Dietary omega-6, but not omega-3, polyunsaturated or saturated fatty acids increase inflammation in primary lung mesenchymal cells. Rutting S, Xenaki D, Lau E, Horvat J, Wood LG, Hansbro PM, Oliver BG. Am J Physiol Lung Cell Mol Physiol. 2018 Jun 1;314(6):L922-L935. doi: 10.1152/ajplung.00438.2017. Epub 2018 Jan 25. PMID: 29368548.
3. Omega-6 fatty acids and inflammation. Innes JK, Calder PC. Prostaglandins Leukot Essent Fatty Acids. 2018 May;132:41-48. doi: 10.1016/j.plefa.2018.03.004. Epub 2018 Mar 22. PMID: 29610056.
4. Red Blood Cell Omega-6 Fatty Acids and Biomarkers of Inflammation in the Framingham Offspring Study. Lai HTM, Ryder NA, Tintle NL, Jackson KH, Kris-Etherton PM, Harris WS. Nutrients. 2025 Jun 22;17(13):2076. doi: 10.3390/nu17132076. PMID: 40647182; PMCID: PMC12251348.

microbial–metabolic signatures associated with plaque destabilization and resolution

Coronary artery disease (CAD) is the primary cause of death worldwide (1). Clinical manifestations of CAD are divided into chronic or stable CAD (sCAD), characterized by gradual artery narrowing, and acute coronary syndromes (ACS), which involve a sudden interruption of blood flow (2).

The human gut hosts trillions of microbes, known as the gut microbiota, which play key roles in metabolism and immune regulation. Its composition, influenced by environment and genetics, and changes in the gut microbiota have been linked to CAD development. Microbial metabolites can also enter circulation and contribute to CAD pathology (3).

Gut-Heart Axis in Coronary Artery Disease

In a recent study researchers explored the role of the gut-heart axis in coronary artery disease: Distinct microbial and metabolic shifts characterize acute coronary syndrome and recovery.  Xu J et al., Imeta. 2025.

Key highlights:

• Changes in the gut microbiome are closely linked to CAD progression.
• Changes are observed across normal coronary arteries, stable CAD, and acute coronary syndrome (ACS).
• Multi-omics machine learning models effectively differentiated CAD subtypes, outperforming traditional clinical risk factors.

 

Our human NT-proBNP assay was featured in this study.

NT-proBNP ELISA (cat. no. SK-1204)

√  CONVENIENT – can be used in every lab

√  RELIABLE – Full validation package

√  EASY – 5 pre-diluted standards and 2 controls included

√  TRUSTED – Widely cited in more than 140 publications 

 

Literature

1. Global prevalence of coronary artery disease: an update from the global burden of disease study. Stark, B, Johnson, C, Roth, G. JACC.2024 Apr, 83 (13_Supplement) 2320.
2. Acute and chronic coronary artery disease. Lancellotti P. Acta Cardiol. 2024 Apr;79(2):105-108. PMID: 38628088.
3. The role of gut microbiota in cardiovascular diseases and their potential as novel therapeutic targets. Yamashita T. J Cardiol. 2025 Aug;86(2):141-147. doi: 10.1016/j.jjcc.2025.05.002. Epub 2025 May 21. PMID: 40409712.
4. Distinct microbial and metabolic shifts characterize acute coronary syndrome and recovery. Xu J et al., Imeta. 2025 Sep 19;4(5):e70079. PMID: 41112052.

Insights from animal models and MSC transplantation

Pulmonary Veno-Occlusive Disease (PVOD), also known as “pulmonary arterial hypertension (PAH), is a rare form of pulmonary hypertension. It is caused by progressive blockage of small veins in the lungs leading to increased pressure followed by right-sided heart failure (1). As effective treatments are limited, lung transplantation remains the only available option. There is no effective medical treatment and lung transplantation is the only curative option. The prognosis is unfavorable, with an average life expectancy of two years following onset of symptoms (2).

Developing PVOD-Specific Therapies

In a recent study researchers investigated the impact of allogeneic mesenchymal stem cell (ASCs) transplantation on lung tissue and its potential in reducing pulmonary hypertension in a rat model of PVOD. Additionally, they assessed whether this intervention contributes to the improvement of right ventricular hypertrophy (3). Continued and future research involving animal models alongside patient samples offers hope for developing PVOD-specific therapies that can prevent and/or treat the disease (4).

Intravenous mesenchymal stem cell transplantation mitigates pulmonary vascular remodeling but poses dose related risks in a pulmonary veno-occlusive disease model.

Abstract

Background: Pulmonary veno-occlusive disease (PVOD) is a rare subtype of disease that causes pulmonary hypertension with vascular involvement of postcapillary structures of pulmonary vasculature. The disease has a poor prognosis with no effective therapy. The study aimed to determine whether adipose-derived mesenchymal stem cells (ASCs) alleviate pulmonary hypertension and right ventricular hypertrophy in a rat model of PVOD.

Methods: Allogeneic ASCs were intravenously administered to a rat model of PVOD induced by mitomycin C. Then, muscularization in pulmonary microvessels, right ventricular systolic pressure (RVSP), and right ventricular hypertrophy were assessed using immunohistochemistry, right heart catheterization, heart weight, and hematoxylin–eosin (HE) staining. Body weight over time and survival rates were assessed.

Results: ASC transplantation substantially contributed to the reduction of pulmonary microvascular muscularization in the PVOD rat model but not to the decrease in RVSP. Furthermore, it led to the attenuation of right ventricular hypertrophy and a considerable decrease in wall thickness. However, repeated ASC administration increased the mortality rate in the PVOD rat models.

Conclusions: To the best of our knowledge, this is the first study to analyze the effects of ASC transplantation in a rat model of PVOD. While intravenous ASC transplantation exerts beneficial effects on the lungs and right ventricle, adverse events may occur depending on the administration method. Therefore, intravenous ASC transplantation should be performed with caution.

 

NT-proBNP measurements were successfully performed in the PVOD rat model in rat serum utilizing our Rat NT-proBNP ELISA assay.

Rat NT-pro BNP ELISA assay (cat. no. BI-1204R)

• Efficient – only 10 µl / well sample
• Accurate – kit control included – protocol booklet click here
• Reliable – sample values provided –  validation data click here
• Trusted – cited using various rat models – citations click here 

Read our first independant review

Rat NT-proBNP ELISA assay

 

Related products:

NT-proANP ELISA Assay (cat. no. BI-20892)

• Small sample volume – 10 µl / well
• Assay suitable for rat and mouse samples – NT-proANP as a cardiovascular safety biomarker in rats Citations

 

Literature:

1. Diagnosis and management of pulmonary veno-occlusive disease. Solinas S, Boucly A, Beurnier A, Kularatne M, Grynblat J, Eyries M, Dorfmüller P, Sitbon O, Humbert M, Montani D. Expert Rev Respir Med. 2023 Jul-Dec;17(8):635-649. doi: 10.1080/17476348.2023.2247989. Epub 2023 Aug 21. PMID: 37578057.
2. Pulmonary Veno-Occlusive Disease. Siddiqui NA, Charoenpong P. 2023 Jul 31. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan–. PMID: 36256776.
3. Intravenous mesenchymal stem cell transplantation mitigates pulmonary vascular remodeling but poses dose related risks in a pulmonary veno-occlusive disease model. Katagiri J, Homma J, Takagi R, Sekine H, Shinkawa T, Niinami H, Shimizu T.Stem Cell Res Ther. 2025 May 28;16(1):258. doi: 10.1186/s13287-025-04400-8. PMID: 40437633; PMCID: PMC12121274.
4. Pulmonary veno-occlusive disease: Insights from animal models. Hata A, Gur B, Kalra J, Prabhakar A. Vascul Pharmacol. 2025 Sep 10;161:107547. doi: 10.1016/j.vph.2025.107547. Epub ahead of print. PMID: 40939813.

Sclerostin is a glycoprotein primarily produced by osteocytes, bone cells embedded within the bone matrix. It plays a crucial role in regulating bone metabolism by acting as Wnt signaling pathway antagonist, essential for promoting bone formation. By inhibiting this pathway, sclerostin effectively reduces osteoblast activity and bone formation, thereby maintaining a balance between bone growth and resorption (1).

Standardizing Sclerostin Measurement

Sclerostin has emerged as a promising therapeutic target for bone-related disorders, particularly osteoporosis. By inhibiting sclerostin, it is possible to enhance Wnt signaling, thereby stimulating osteoblast activity and promoting new bone formation. This approach aims to counteract the excessive bone loss characteristic of osteoporosis and other metabolic bone diseases. Several sclerostin inhibitors have been developed, with romosozumab being the most notable. Romosozumab is a monoclonal antibody that binds to sclerostin, effectively neutralizing its activity (2, 3).

Sclerostin and Type 2 Diabetes Mellitus

Epidemiological studies have reported that Type 2 diabetes (T2D) is linked to a higher risk of fractures (4). In addition, Sclerostin has been shown to be associated with fasting insulin levels and homoeostatic model assessment-insulin resistance (HOMA-IR) (5). Numerous studies have demonstrated increased circulating Sclerostin levels in T2D patients (6, 7). Furthermore, serum sclerostin levels also correlate with the duration of T2DM, glycated hemoglobin, bone turnover markers, and BMD in T2DM patients (6). Elevated Sclerostin levels have been linked to a higher risk of vertebral fractures in T2DM patients, regardless of BMD and bone turnover, indicating that sclerostin may reflect bone fragility related to deteriorated bone quality within gender-specific BMD T-score ranges (8).

A recent study by Traechslin C et al. (7), investigated the association of total and bioactive serum Sclerostin levels with bone metabolism in type 2 diabetes mellitus (T2DM) using three different Sclerostin ELISA assays.

Key highlights:

• Identifying diabetes patients at risk for fragility fractures is challenging.
• Sclerostin levels are significantly increased in T2DM, particularly in men when bioactive Sclerostin is measured.
• Significant positive correlation between serum Sclerostin and Bone Mineral Density-Sclerostin could be a useful marker in evaluating bone fragility in T2DM patients.
• Bioactive sclerostin more accurately reflects bone metabolism based on clinical findings.

 

These findings are an initial step to standardize sclerostin measurement to evaluate bone metabolism.

Bioactive Sclerostin ELISA (cat. no. BI-20472)

• CHARACTERIZED ANTIBODIES – targeting the receptor binding region
• TRUSTED – validated for clinical samples  (validation data file)
• LOW sample volume – 20µl sample /well (protocol booklet)

 

Bioactive SCLEROSTIN ELISA – Binding Sites of antibodies utilized in the assay

 

 

Sclerostin ELISA (cat. no. BI-20492)

• TRUSTED – most referenced
• LOW sample volume – 20µl sample /well (protocol booklet)
• RELIABLE – validated  following international quality guidelines

 

 

 

Association of total and bioactive serum sclerostin levels with bone metabolism in type 2 diabetes mellitus. Traechslin C et al, Clin Transl Endocrinol; 2025.

Abstract

Background: Sclerostin has been associated with decreased bone turnover in patients with type 2 diabetes mellitus (T2DM). The relationship with bone turnover markers (BTMs) and bone mineral density (BMD) remains unclear. We investigate the relationship between total and bioactive sclerostin measured by three different assays with BTMs and BMD in patients with T2DM compared to healthy controls.

Methods: Baseline data from the cross-sectional multicenter DiabOS-study in Switzerland were analysed. Total and bioactive serum sclerostin levels were measured using three different ELISA-based sclerostin assays (Sclerostin Biomedica, Sclerostin bioactive Biomedica and Sclerostin hsTECO). Sclerostin levels in patients with T2DM and controls were correlated with BTMs and BMD.

Results: Data were analysed from 78 men and postmenopausal women with T2DM and 37 controls (aged 50-75 years). Serum sclerostin levels, adjusted for estimated glomerular filtration rate (eGFR), were higher in patients with T2DM compared to controls with all three assays. In a gender subgroup analysis, bioactive sclerostin levels remained significantly elevated in men with T2DM (T2DM, 106.8 ± 39.9 pmol/L; controls, 88.3 ± 21.3 pmol/L, p = 0.03).Univariate analysis showed consistent significant correlations with all sclerostin assays for age, eGFR, glycated hemoglobin A1c and diabetes duration. However, in multivariate analysis, eGFR remained the only significant determinant of serum sclerostin levels. Sclerostin levels in patients with T2DM showed significant positive correlations with BMD but no significant correlations with BTMs.

Conclusions: We demonstrate a significant positive association of bioactive serum sclerostin with BMD at all measured sites in patients with T2DM, which may support its utility in the assessment of bone fragility in this population.

Literature

1. Sclerostin: From Molecule to Clinical Biomarker. Omran A, Atanasova D, Landgren F, Magnusson P. Int J Mol Sci. 2022 Apr 26;23(9):4751. doi: 10.3390/ijms23094751. PMID: 35563144; PMCID: PMC9104784.
2. A practical approach for anabolic treatment of bone fragility with romosozumab. Cianferotti L, Cipriani C, Palermo A, Viapiana O, Zavatta G, Mazziotti G.J Endocrinol Invest. 2024 Nov;47(11):2649-2662. doi: 10.1007/s40618-024-02395-2. Epub 2024 May 24. PMID: 38789679.
3. Romosozumab. Krupa KN, Parmar M, Delo LF. 2024 Jul 19. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan–. PMID: 36256789.
4. Skeletal Fragility in Type 2 Diabetes Mellitus. Starup-Linde J, Hygum K, Langdahl BL.Endocrinol Metab (Seoul). 2018 Sep;33(3):339-351. doi: 10.3803/EnM.2018.33.3.339. PMID: 30229573; PMCID: PMC6145952.
5. The association between sclerostin and incident type 2 diabetes risk: a cohort study. Yu OH, Richards B, Berger C, Josse RG, Leslie WD, Goltzman D, Kaiser SM, Kovacs CS, Davison KS. Clin Endocrinol (Oxf). 2017 Apr;86(4):520-525. doi: 10.1111/cen.13300. Epub 2017 Jan 26. PMID: 28090669.
6. Circulating levels of sclerostin are increased in patients with type 2 diabetes mellitus. García-Martín A, Rozas-Moreno P, Reyes-García R, Morales-Santana S, García-Fontana B, García-Salcedo JA, Muñoz-Torres M. J Clin Endocrinol Metab. 2012 Jan;97(1):234-41. doi: 10.1210/jc.2011-2186. Epub 2011 Oct 26. PMID: 22031520.
7. Circulating sclerostin levels and bone turnover in type 1 and type 2 diabetes. Gennari L, Merlotti D, Valenti R, Ceccarelli E, Ruvio M, Pietrini MG, Capodarca C, Franci MB, Campagna MS, Calabrò A, Cataldo D, Stolakis K, Dotta F, Nuti R. J Clin Endocrinol Metab. 2012 May;97(5):1737-44. doi: 10.1210/jc.2011-2958. Epub 2012 Mar 7. PMID: 22399511.
8. Elevated sclerostin levels are associated with vertebral fractures in patients with type 2 diabetes mellitus. Yamamoto M, Yamauchi M, Sugimoto T. J Clin Endocrinol Metab. 2013 Oct;98(10):4030-7. doi: 10.1210/jc.2013-2143. Epub 2013 Jul 26. PMID: 23894157.
9. Association of total and bioactive serum sclerostin levels with bone metabolism in type 2 diabetes mellitus. Traechslin C, Sewing L, Baumann S, Grize L, Vavanikunnel J, Kraenzlin M, Henzen C, Meier C.J Clin Transl Endocrinol. 2025 Apr 8;40:100393. doi: 10.1016/j.jcte.2025.100393. PMID: 40275939; PMCID: PMC12019839.

 

 

 

About Dickkopf-1 (DKK-1)  – a  key regulator of the Wnt signaling pathway

DKK-1 is a protein that functions as a key regulator of the Wnt signaling pathway, which is essential for various cellular processes including growth, development, and tissue homeostasis. DKK-1 primarily acts as an antagonist of the Wnt pathway by binding to specific receptors, thereby inhibiting Wnt signaling activity.

The Wnt pathway is a complex and highly conserved signaling cascade that plays a crucial role in regulating cell growth, differentiation, migration, and tissue development. It also plays a critical role in bone biology, particularly in the regulation of bone formation and remodeling as it influences the activity of osteoblasts, the cells responsible for building new bone, and helps maintain bone mass and strength.

DKK-1 linked to poor prognosis and metastasis in breast cancer

DKK-1 a potential biomarker for disease progression in breast cancer

DKK-1 plays a crucial role in breast cancer by modulating the Wnt signaling pathway, which regulates cell proliferation, differentiation, and migration. Abnormal expression of DKK-1 has been detected in breast cancer, with elevated levels often associated with tumor progression and metastasis, especially to the bones. Increased DKK-1 expression has been linked to poorer prognosis and a higher risk of bone metastases, as it affects the tumor microenvironment and bone remodeling processes (1-3). Therefore, DKK-1 is regarded as a potential biomarker for disease progression and a promising target for therapeutic strategies in breast cancer treatment (4, 5).

DKK-1 suppresses NK cell cytotoxicity in breast cancer

Breast cancer patients with progressive bone metastases exhibit higher levels of DKK-1 and a decreased number of cytotoxic NK cells compared to those with stable disease. Recent findings suggest that DKK1 promotes a tumor-supporting environment by suppressing NK cell activity in breast cancer (6).

Breast cancer is minimally immunogenic, which allows it to evade T cell recognition and results in limited responsiveness to immune checkpoint blockade. Additionally, breast cancer cells can evade NK cell-mediated immune surveillance. Recent findings suggest that DKK-1 promotes a tumor-supporting environment in breast cancer by suppressing NK cell function (7).

Stroma-derived Dickkopf-1 contributes to the suppression of NK cell cytotoxicity in breast cancer .  Lee S et al., 2025; Nat Commun.

Abstract

Mechanisms related to tumor evasion from NK cell-mediated immune surveillance remain enigmatic. Dickkopf-1 (DKK1) is a Wnt/β-catenin inhibitor, whose levels correlate with breast cancer progression. We find DKK1 to be expressed by tumor cells and cancer-associated fibroblasts (CAFs) in patient samples and orthotopic breast tumors, and in bone. By using genetic approaches, we find that bone-derived DKK1 contributes to the systemic DKK1 elevation in tumor-bearing female mice, while CAFs contribute to DKK1 at primary tumor site. Systemic and bone-specific DKK1 targeting reduce tumor growth. Intriguingly, deletion of CAF-derived DKK1 also limits breast cancer progression, without affecting its levels in circulation, and regardless of DKK1 expression in the tumor cells. While not directly supporting tumor proliferation, stromal-DKK1 suppresses NK cell activation and cytotoxicity by downregulating AKT/ERK/S6 phosphorylation. Importantly, increased DKK1 levels and reduced cytotoxic NK cells are detected in women with progressive breast cancer. Our findings indicate that DKK1 represents a barrier to anti-tumor immunity through suppression of NK cells.

DKK-1 can reliably be measured in biological fluids with a conventional ELISA assay.

DKK-1 ELISA Assay Highlights (Cat. No. BI-20413)

• Small sample volume – 10 µl / well
• Direct measurement- no pre-dilution of samples required!
• Reliable – full validation package
• Easy – 6 standards and control included
• Trusted – widely cited in more than 180 publications
• Protocol booklet link

 

Download our DKK-1 Leaflet here

 

 

 

Literature

1. Increased Dickkopf-1 expression in breast cancer bone metastases. Voorzanger-Rousselot N, Goehrig D, Journe F, Doriath V, Body JJ, Clézardin P, Garnero P. Br J Cancer. 2007 Oct 8;97(7):964-70. doi: 10.1038/sj.bjc.6603959. Epub 2007 Sep 18. PMID: 17876334; PMCID: PMC2360424.
2. Serum Dickkopf-1 acts as a new biomarker in human breast cancer. Liu JT, Guo WB, Sun JY. Minerva Med. 2017 Aug;108(4):334-340. doi: 10.23736/S0026-4806.17.04807-8. Epub 2017 Mar 1. PMID: 28248066.
3. Dickkopf-1: A Promising Target for Cancer Immunotherapy. Chu HY, Chen Z, Wang L, Zhang ZK, Tan X, Liu S, Zhang BT, Lu A, Yu Y, Zhang G. Front Immunol. 2021 May 20;12:658097. doi: 10.3389/fimmu.2021.658097. PMID: 34093545; PMCID: PMC8174842.
4. Dickkopf-1 as a mediator and novel target in malignant bone disease. Rachner TD, Göbel A, Benad-Mehner P, Hofbauer LC, Rauner M. Cancer Lett. 2014 May 1;346(2):172-7. doi: 10.1016/j.canlet.2014.01.010. Epub 2014 Jan 22. PMID: 24462802.
5. Dkk1 as a Prognostic Marker for Neoadjuvant Chemotherapy Response in Breast Cancer Patients. Kasoha M, Steinbach AK, Bohle RM, Linxweiler B, Haj Hamoud B, Doerk M, Nigdelis MP, Stotz L, Zimmermann JSM, Solomayer EF, Kaya AC, Radosa JC. Cancers (Basel). 2024 Jan 18;16(2):419. doi: 10.3390/cancers16020419. PMID: 38254908; PMCID: PMC10814026.
6. Cancer-associated fibroblast-derived Dickkopf-1 suppresses NK cell cytotoxicity in breast cancer. Faccio R, Lee S, Ricci B, Tran J, Ye J, Clever D, Eul E, Wang J, Wong P, Ma C, Fehniger T. Res Sq [Preprint]. 2024 Apr 8:rs.3.rs-4202878. doi: 10.21203/rs.3.rs-4202878/v1. Update in: Nat Commun. 2025 Jan 30;16(1):1183. doi: 10.1038/s41467-025-56420-w. PMID: 38659818; PMCID: PMC11042392.
7. Stroma-derived Dickkopf-1 contributes to the suppression of NK cell cytotoxicity in breast cancer. Lee S, Ricci B, Tran J, Eul E, Ye J, Ren Q, Clever D, Wang J, Wong P, Haas MS, Stewart SA, Ma CX, Fehniger TA, Faccio R. Nat Commun. 2025 Jan 30;16(1):1183. doi: 10.1038/s41467-025-56420-w. PMID: 39885132; PMCID: PMC11782527.

 

During Breast Cancer Awareness Month, let´s share insights on emerging biomarkers such as PERIOSTIN that offer potential for improved diagnosis, prognosis, and personalized therapy.

PERIOSTIN is a potential marker for breast cancer progression

 Periostin is a matricellular protein that plays a significant role in the progression of breast cancer. Several studies have demonstrated that Periostin is overexpressed in breast cancer tissues compared to normal breast tissue (1, 2). In addition, breast tumor progression has been shown to be accompanied by increased Periostin expression; researchers could show that elevated Periostin expression in epithelial cells was linked to decreased disease-free survival and overall survival (3). These findings suggest that Periostin plays a significant role in breast tumor progression.

 

High circulating Periostin levels are associated with aggressive breast cancer subtypes and poorer patient prognosis

Periostin is involved in various processes such as tumor growth, invasion, metastasis, and the modulation of the tumor microenvironment (4). High serum Periostin levels have been associated with more aggressive breast cancer subtypes and poorer patient prognosis (5). Periostin promotes tumor cell survival, supports angiogenesis, and facilitates the remodeling of the extracellular matrix, thereby aiding cancer cell dissemination (5).

 

Periostin significantly impacts cancer progression and treatment outcomes

Periostin plays vital roles in tumor development, metastasis, resistance to chemotherapy, and shaping the tumor microenvironment (6). In addition, Periostin contributes to chemotherapy resistance by creating a protective niche for cancer cells (6). In a recent study researchers explored the relationship between Periostin and the tumor microenvironment, highlighting its potential as a promising prognostic biomarker and therapeutic target for addressing tumor progression and chemoresistance (7). In a further study researchers aimed to identify proteins that are overexpressed in tumors with extensive stroma within immune-excluded triple-negative breast cancer, revealing a link between Periostin and elevated tumor stroma along with immune exclusion in triple-negative breast cancer (8).

Periostin can reliably be measured in biological fluids with a conventional ELISA assay

Periostin ELISA Assay Highlights (Cat. No. BI-20433)

• Small sample volume – 10 µl / well
• Reliable – full validation package
• Easy – 7 standards and 2 controls included
• Trusted – widely cited 

 

Download our Periostin Flyer here

 

 

Literature

1. Expression of periostin in human breast cancer. Puglisi F, Puppin C, Pegolo E, Andreetta C, Pascoletti G, D’Aurizio F, Pandolfi M, Fasola G, Piga A, Damante G, Di Loreto C. J Clin Pathol. 2008 Apr;61(4):494-8. doi: 10.1136/jcp.2007.052506. Epub 2007 Oct 15. PMID: 17938160.
2. The expression analysis of periostin in human breast cancer. Zhang Y, Zhang G, Li J, Tao Q, Tang W. J Surg Res. 2010 May 1;160(1):102-6. doi: 10.1016/j.jss.2008.12.042. Epub 2009 Feb 27. PMID: 19524268.
3. Epithelial periostin expression is correlated with poor survival in patients with invasive breast carcinoma. Kim GE, Lee JS, Park MH, Yoon JH. PLoS One. 2017 Nov 21;12(11):e0187635. doi: 10.1371/journal.pone.0187635. PMID: 29161296; PMCID: PMC5697858.
4. Periostin: biology and function in cancer. Dorafshan S, Razmi M, Safaei S, Gentilin E, Madjd Z, Ghods R. Cancer Cell Int. 2022 Oct 12;22(1):315. doi: 10.1186/s12935-022-02714-8. PMID: 36224629; PMCID: PMC9555118.
5. High serum levels of periostin are associated with a poor survival in breast cancer. Rachner TD, Göbel A, Hoffmann O, Erdmann K, Kasimir-Bauer S, Breining D, Kimmig R, Hofbauer LC, Bittner AK. Breast Cancer Res Treat. 2020 Apr;180(2):515-524. doi: 10.1007/s10549-020-05570-0. Epub 2020 Feb 10. PMID: 32040688.
6. The roles of periostin derived from cancer-associated fibroblasts in tumor progression and treatment response. De Oliveira Macena Y, Cezar MEN, Lira CBF, De Oliveira LBDM, Almeida TN, Costa ADAV, De Araujo BMD, de Almeida Junior D, Dantas HM, De Mélo EC, de Araújo ST, de França Júnior RR, Dos Santos Lemos Gurgel MA, de Carvalho Fraga CA. Cancer Metastasis Rev. 2024 Nov 30;44(1):11. doi: 10.1007/s10555-024-10233-3. PMID: 39614015.
7. The association between periostin and tumor microenvironment: a promising cancer prognostic biomarker and therapeutic target to combat tumor progression and chemoresistance. Nabi-Afjadi M, Farzam F, Soltani S, Golestani N, Asl SS, Aziziyan F, Zalpoor H, Ghasemi F, Dabirmanesh B, Khajeh K. Cancer Cell Int. 2025 Sep 3;25(1):320. doi: 10.1186/s12935-025-03959-9. PMID: 40903761; PMCID: PMC12406393.

Breast Cancer Awareness Month is an international health campaign, dedicated to increasing awareness about screening and prevention for a disease that affects approximately 2.3 million women worldwide (1).

Breast cancer is the most common cancer among women and the leading most common cancer diagnosis (2). Although it mainly affects women, men can also develop malignant breast tissue (3). Male breast cancer is rare, making up about 1% of all cases, but men are often diagnosed at more advanced stages. This delay in seeking medical attention frequently results in later detection and less favorable outcome.

OCTOBER BREAST CANCER AWARENESS MONTH

Detecting breast cancer early greatly enhances the chances of successful treatment, resulting in higher survival rates, less intensive therapies, and improved quality of life. Key early detection strategies include routine mammograms, clinical breast exams, and being attentive (4) .Early detection of breast cancer significantly improves successful outcomes by leading to higher survival rates, less aggressive treatment options, and a better quality of life (4).

Learn about Personalized Early Detection and Prevention of Breast Cancer:

– Breast cancer: A review of risk factors and diagnosis. Medicine (Baltimore). Obeagu EI et al.,  2024.   

– Breast Cancer Awareness Month 2025 UK | Breast Cancer Now

– October is Breast Cancer Awareness Month – American Association of Cancer Research 

– Breast Cancer Awareness Month 2025, World Health Organization

– Personalized early detection and prevention of breast cancer: ENVISION consensus statement. Pashayan N et al.,  2020.

Abstract

The European Collaborative on Personalized Early Detection and Prevention of Breast Cancer (ENVISION) brings together several international research consortia working on different aspects of the personalized early detection and prevention of breast cancer. In a consensus conference held in 2019, the members of this network identified research areas requiring development to enable evidence-based personalized interventions that might improve the benefits and reduce the harms of existing breast cancer screening and prevention programmes. The priority areas identified were: 1) breast cancer subtype-specific risk assessment tools applicable to women of all ancestries; 2) intermediate surrogate markers of response to preventive measures; 3) novel non-surgical preventive measures to reduce the incidence of breast cancer of poor prognosis; and 4) hybrid effectiveness-implementation research combined with modelling studies to evaluate the long-term population outcomes of risk-based early detection strategies. The implementation of such programmes would require health-care systems to be open to learning and adapting, the engagement of a diverse range of stakeholders and tailoring to societal norms and values, while also addressing the ethical and legal issues. In this Consensus Statement, we discuss the current state of breast cancer risk prediction, risk-stratified prevention and early detection strategies, and their implementation. Throughout, we highlight priorities for advancing each of these areas.

 

BIOMEDICA offers fully validated Biomarker ELISA Kits for Breast Cancer Research

PERIOSTIN ▪ NEUROPILIN-1 ▪ OSTEPROTEGERIN ▪ soluble RANKL ▪ SEMAPHORIN 4D ▪ IL-6

click here for more information on our Biomarker ELISAs in Oncology

 

ELISA Assay Kit Highlights

• EASY –ready to use calibrators & controls included (color-coded reagents)
• FULL VALIDATION PACKAGE – assays are optimized for clinical samples
• HIGH QUALITY GUARANTEED – results you can rely on
• WIDELY CITED in over 1000 publications

 

BIOMEDICA – Complete ready-to-use ELISA kits for superior performance and reproducibility

 

 

Literature

1. Breast Cancer Awareness Month 2025, World Health Organization
2. Breast cancer: presentation, investigation and management. Katsura C, Ogunmwonyi I, Kankam HK, Saha S. Br J Hosp Med (Lond). 2022 Feb 2;83(2):1-7. doi: 10.12968/hmed.2021.0459. PMID: 35243878.
3. Male Breast Cancer. Khattab A, Kashyap S, Monga DK. 2024 Sep 10. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan–. PMID: 30252292.

 

 

 

World Heart Day 2025 is a global initiative dedicated to raising awareness about cardiovascular health. It highlights the importance of healthy living to prevent heart disease and stroke.  

Biomarkers have revolutionized on how heart diseases are diagnosed and treated. Ongoing research on newer exploratory protein biomarkers may shed light into the complex mechanisms that drive the disease process.

Biomedica offers a range of quality ELISA assay kits for your clinical and preclinical research:

World Heart Day – September 29, 2025

Biomarkers for Heart Disease:  NT-proBNP, NT-proAN`P, Big Endothelin-1, FGF23, LRG1

NT-proBNP  is a biomarker used to assess heart failure and measure the severity of cardiac dysfunction. Elevated levels of NT-proBNP indicate increased stress on the heart (1).

NT-proANP (N-terminal pro-atrial natriuretic peptide) is a biomarker released by the heart in response to atrial stretch and increased blood volume. It is used clinically to assess heart failure and identify cardiac stress, aiding in diagnosis and management of cardiovascular conditions (2).

Big Endothelin-1 is an inactive precursor of endothelin-1, a potent vasoconstrictor involved in regulating blood vessel tone and blood pressure. Elevated levels of Big Endothelin-1 are associated with cardiovascular diseases such as hypertension and heart failure (3).

FGF23 (Fibroblast Growth Factor 23) is a hormone primarily involved in regulating phosphate metabolism and vitamin D levels. It helps maintain mineral balance by reducing phosphate reabsorption in the kidneys and suppressing vitamin D activation. Elevated FGF23 levels are linked to cardiovascular disease and chronic kidney disease (4).

Leucine-rich alpha-2-glycoprotein (LRG) is a plasma protein involved in immune response and inflammation. It plays a role in modulating immune cell activity and has been studied as a potential biomarker for various inflammatory and infectious conditions (5).

 

Biomedica offers a range of quality ELISA assay kits for your clinical and preclinical research:

-NT-proBNP (Cat. No. BI-1204), Rat NT-proBNP (Cat. No. BI-1204R)

-NT-proANP (Cat. No. BI-20892) (human  and non-human (rat, mouse.. ) use

-Big Endothelin-1 (Cat. No. BI-20082H)

-FGF23 intact (Cat. No. BI-20700)

-FGF23 c-terminal (Cat. No.  BI-20702)

-LRG (Cat. No. BI-LRG)

 

Literature 

1. BNP and NT-proBNP as prognostic biomarkers for the prediction of adverse outcomes in HFpEF patients: A systematic review and meta-analysis. Ammar LA, Massoud GP, Chidiac C, Booz GW, Altara R, Zouein FA. Heart Fail Rev. 2025 Jan;30(1):45-54. doi: 10.1007/s10741-024-10442-6. Epub 2024 Oct 7. PMID: 39373821; PMCID: PMC12002167.
2. Prognostic value of NT-proANP levels on major cardiovascular outcomes in a 31-year follow-up study depends on baseline morbidity. Sakko S, Perkiömäki J, Ylitalo A, Huikuri H, Ukkola O, Koivunen P, Tapio J. Sci Rep. 2025 May 28;15(1):18660. doi: 10.1038/s41598-025-03819-6. PMID: 40436983; PMCID: PMC12119872.
3. Prognostic Value of Plasma Big Endothelin-1 in Patients Hospitalized for Heart Failure. Wang J, Feng J, Tse G, Zhai M, Huang Y, Zhou Q, Zhuang X, Liu H, Zhang Y, Zhang J. Korean Circ J. 2025 Aug;55(8):705-717. doi: 10.4070/kcj.2024.0354. Epub 2025 Apr 11. PMID: 40345830; PMCID: PMC12314060.
4. Network Interactions of Circulating FGF23, HRG-HMGB1, and Cardiac Disease in CKD. Perwad F, Akwo EA, Singhal A, Vartanian N, Suva LJ, Friedman PA, Robinson-Cohen C. J Am Soc Nephrol. 2025 Apr 16. doi: 10.1681/ASN.0000000710. Epub ahead of print. PMID: 40238264.
5. Leucine-rich alpha-2 glycoprotein as a potential biomarker for large vessel vasculitides. Umezawa N, Mizoguchi F, Maejima Y, Kimura N, Hasegawa H, Hosoya T, Fujimoto M, Kohsaka H, Naka T, Yasuda S. Front Med (Lausanne). 2023 May 5;10:1153883. doi: 10.3389/fmed.2023.1153883. PMID: 37215715; PMCID: PMC10196172.

Our EZ4U (easy for you) cell proliferation and cytotoxicity assay was highlighted in a recent study that investigated the use of peptidomimetics, selected synthetic small-molecule compounds, as a therapeutic approach for the targeted treatment of neurodegenerative conditions such as Alzheimer’s disease.

The use of selected peptidomimetics has shown strong inhibitory effects on amyloid protein aggregation, highlighting their potential as promising therapeutic candidates.

Alzheimer´s Research with EZ4U Cell Viability Assay

Protective Effect of a Hexapeptide Derived from Rotifer-Specific SCO-Spondin Against Beta-Amyloid Toxicity. Datki Z, Sinka R, Dingmann BJ, Galik B, Szabo A, Galik-Olah Z, Toth GK, Bozso Z. Int J Mol Sci. 2025 May 26;26(11):5109. doi: 10.3390/ijms26115109. PMID: 40507923; PMCID: PMC12154537.

Abstract

The Rotimer (rotifer-specific biopolymer) like SCO-spondin (R-SSPO/1), predicted as the main component of this biopolymer, is an adequate base for the design of functional small peptides. This macromolecule is interactive and protective against neurotoxic human-type beta-amyloid 1-42 aggregates (agg-Aβ). The current work presents biological investigations and predictable molecular interaction analysis of DSSNDL and PNCRDGSDE peptides that were synthesized based on the sequences of R-SSPO/1. Viability assays (NADH-dependent cellular reduction capacity, intracellular esterase activity, and motility) were performed on differentiated neuro-type cell cultures (SH-SY5Y and PC12) and on Rotimer-depleted rotifers (Euchlanis dilatata and Lecane bulla). A control peptide (STTRPTGTT), not found in Rotimer, was also included in the study. All three peptides are present in both rotifer and human proteomes. Among these small molecules, DSSNDL showed a significant protective effect against the toxicity of agg-Aβ both in vitro and in vivo and presumably interacted with its aggregates. The stagogram analysis of amyloid-peptide complexes and the possible bonding competition of these small molecules against aggregation-specific dyes on agg-Aβ surface suggest that DSSNDL affects the properties of these neurotoxic macromolecules. This effective hexapeptide can serve as a promising candidate for further investigations into the inactivation of beta-amyloid toxicity.

Analysis of Cell Viability

The toxicity of aggregated Aβ and the impact of potential antagonistic peptides were examined. Mitochondrial and cytoplasmic reduction capacities were assessed using the EZ4U kit, which measures soluble formazan produced after 4 hours of incubation; the absorbance at 490/630 nm correlates with cell viability in the samples.

 

Alzheimer´s Research with EZ4U Cell Viability Assay

EZ4U Kit (cat.no. BI-5000)

– Non-radioactive & non-toxic assay

– Reliable & sensitive

– Convenient single-step incubation-for use on living #cells

– Widely cited in more than 290 publications

 

In Chronic Kidney Disease (CKD), fibroblast growth factor 23 (FGF23) acts as a cardiovascular toxin by contributing to hypertension, vascular calcification, and left ventricular hypertrophy, leading to increased cardiovascular risk and mortality (1). 

FGF23 clearance in hemodialysis patients

In a recent study researchers explored whether the use of different dialysis membranes result in a reduction of FGF23 and other inflammatory cytokine levels (IL-6, IL-18, dp-ucMGP, and hsCRP) in hemodialysis patients.

A Randomised Prospective Crossover Study on the Effects of Medium Cut-Off Membranes on FGF-23 and Inflammatory Mediators in Patients Receiving Regular Haemodialysis. Al-Chalabi S, et al., 2025. Blood Purif.

Abstract

Introduction: In contrast to high-flux dialysis (HFD) membranes, medium cut-off membranes (MCO) can potentially remove a wide range of middle molecules. Our study aimed to compare the clearance rate (CR) of fibroblast growth factor 23 (FGF-23) and other selected inflammatory cytokines between medium MCO and HFD membranes and investigate the intrasubject stability of these biomarkers.

Methods: This prospective randomised case-crossover study recruited 20 adult patients who were randomised into two groups: group A: to start with 1 week of thrice-weekly dialysis using HFD membrane followed by a 3-week washout period and then 1 week of dialysis with an MCO membrane. Group B followed the reverse sequence. Blood samples were taken before and after each dialysis session for the analysis of the assessed biomarkers (FGF-23, interleukin-6 [IL-6], interleukin-18 [IL-18], high-sensitivity C-reactive protein [hsCRP], and dephosphorylated uncarboxylated matrix Gla protein [dp-ucMGP]). Wilcoxon signed rank and paired t tests were used for comparison between the membranes. One-way repeated measures ANOVA or Friedman tests were used for the intrasubject stability of the biomarkers.

Results: The use of both MCO and HFD membranes resulted in a significant reduction of FGF-23 levels and other selected inflammatory cytokines. However, there was no significant difference in the CR: FGF-23 (0.31 vs. 0.23], p = 0.242), IL-6 (0.19 vs. 0.12, p = 0.215), IL-18 (-0.05 vs. -0.03, p = 0.704), dp-ucMGP (0.33 vs. 0.33, p = 0.903), and hsCRP (-0.05 vs. -0.08, p = 0.107). There was no significant intrasubject variability for all assessed biomarkers except in pre-dialysis high hsCRP levels when using HFD membrane.

Conclusion: The use of both MCO and HFD membranes resulted in a significant reduction of FGF-23 levels and other selected inflammatory cytokines. However, the MCO membrane did not demonstrate a significant advantage over the HFD in the short term. There was no significant intrasubject variability for all assessed biomarkers apart from hsCRP.

 

BIOMEDICA´s FGF23 and IL-6 ELISA Assay Kits were successfully utilized in the study:

 

FGF23 (C-terminal) multi-matrix ELISA Kit | BI-20702

• Instructions for use
• Validation data file
• Citations

 

IL-6 (Interleukin-6) ELISA Kit | BI-IL6

• Instructions for use
• Validation data file
• Citations

 

 

Related Products:

-Intact FGF23 ELISA Kit | BI-20700

–NT-proBNP ELISA | SK-1204

 

Literature

1. FGF23 and Phosphate-Cardiovascular Toxins in CKD. Toxins (Basel). Vogt I, Haffner D, Leifheit-Nestler M. 2019 Nov 6;11(11):647. doi: 10.3390/toxins11110647. PMID: 31698866; PMCID: PMC6891626.
2. A Randomised Prospective Crossover Study on the Effects of Medium Cut-Off Membranes on FGF-23 and Inflammatory Mediators in Patients Receiving Regular Haemodialysis. Al-Chalabi S, Sinha S, Kalra PA, Evans D, Green D, Schurgers L, Poulikakos D. Blood Purif. 2025 Apr 21:1-13. doi: 10.1159/000545745. Epub ahead of print. PMID: 40258362; PMCID: PMC12105827.

September is Blood Cancer Awareness Month raising awareness about the various types of blood cancers, including leukemia, lymphoma, multiple myeloma, and other hematologic malignancies. The goal of this initiative is to educate the public about the symptoms and the importance of early detection and treatment.

Multiple myeloma (MM) is the second most common blood cancer and the most prevalent type of cancer affecting the bones.

MM-related bone disease (MMBD) has severe implications for patients, leading to significant bone loss, intense bone pain, and pathological fractures that greatly impair quality of life and influence survival outcomes. Multiple myeloma bone disease (MMBD) results from disrupted bone remodeling, marked by increased activity of osteoclasts, breaking down bone and decreased activity of osteoblasts (1, 2).

September is Blood Cancer Awareness Month

Daratumumab is a monoclonal antibody used primarily in the treatment of multiple myeloma. It works by targeting a specific protein called CD38, which is highly expressed on the surface of myeloma cells. By binding to CD38, daratumumab helps the immune system recognize and attack the cancer cells, leading to their destruction. Daratumumab is often used in combination with other therapies and has shown significant effectiveness in improving response rates and survival outcomes for patients with multiple myeloma. It is administered via intravenous infusion and may be associated with side effects such as infusion reactions, fatigue, nausea, and increased risk of infections (3).

In the “REBUILD” Study researchers investigated how Daratumumab impacts bone metabolism in patients with relapsed or refractory multiple myeloma. The Phase 2 “REBUILD” trial aims to assess whether treatment with daratumumab can improve bone turnover markers and potentially help repair bone damage associated with the disease. The findings suggest that Daratumumab not only targets myeloma cells but may also positively influence bone health in affected patients (3)

Daratumumab Improves Bone Turnover in Relapsed/Refractory Multiple Myeloma; Phase 2 Study “REBUILD”. Terpos E et al., .Cancers (Basel). 2022.  

Abstract

Biomarkers of bone turnover in serum are suggestive of bone dynamics during treatment in multiple myeloma (MM). We evaluated the role of daratumumab on bone remodeling among patients with relapsed/refractory MM in the prospective, open-label, phase 2 study REBUILD. Daratumumab was administered according to the approved indication. A total of 33 out of 57 enrolled patients completed 4 months of treatment. The median percent change from baseline to 4 months in C-terminal cross-linking telopeptide of type 1 collagen (CTX) (primary endpoint) was 3.9%, with 13 (39.4%) and 11 (33.3%) patients showing at least 20% and 30% reduction in CTX levels, respectively. The median percent decrease from baseline to 4 months in tartrate resistant acid phosphatase 5b (TRACP-5b) levels (co-primary endpoint) was 2.6%, with 10 (30.3%) and 6 (18.2%) patients showing at least 20% and 30% reduction in TRACP-5b levels, respectively. However, the changes in these markers of bone catabolism were not statistically significant. Furthermore, the levels of osteocalcin, bone-specific alkaline phosphatase and procollagen type-I N-pro-peptide (bone formation markers) increased from baseline to 4 months (secondary endpoints) by 18.4%, 92.6% and 10.2%, respectively. Furthermore, the median levels of dickkopf-1 and C-C motif ligand-3 showed a significant decrease at 4 months by 17.5% and 16.0%, respectively. In conclusion, daratumumab improved bone turnover by inducing bone formation and reducing osteoblast inhibition.

 Evaluation of Bone Remodeling

The following serum markers of bone metabolism were measured with

Biomedica ELISA assays:

• Soluble RANKL (BI-20462)
• Osteoprotegerin – OPG (BI-20403)
• Sclerostin (BI-20492)
• Dickkopf-1 – DKK-1 (BI-20413)

 

Discover our Biomarker ELISA Kit Collection

 

Literature

1. Multiple myeloma. Nat Rev Dis Primers. Malard F, Neri P, Bahlis NJ, Terpos E, Moukalled N, Hungria VTM, Manier S, Mohty M.2024 Jun 27;10(1):45. doi: 10.1038/s41572-024-00529-7. PMID: 38937492.
2. Multiple Myeloma and Bone: The Fatal Interaction. Marino S, Roodman GD. Cold Spring Harb Perspect Med. 2018 Aug 1;8(8):a031286. doi: 10.1101/cshperspect.a031286. PMID: 29229668; PMCID: PMC6071546.
3. Daratumumab or Active Monitoring for High-Risk Smoldering Multiple Myeloma. Dimopoulos MA, Voorhees PM, Schjesvold F, Cohen YC, Hungria V, Sandhu I, Lindsay J, Baker RI, Suzuki K, Kosugi H, Levin MD, Beksac M, Stockerl-Goldstein K, Oriol A, Mikala G, Garate G, Theunissen K, Spicka I, Mylin AK, Bringhen S, Uttervall K, Pula B, Medvedova E, Cowan AJ, Moreau P, Mateos MV, Goldschmidt H, Ahmadi T, Sha L, Cortoos A, Katz EG, Rousseau E, Li L, Dennis RM, Carson R, Rajkumar SV; AQUILA Investigators. N Engl J Med. 2025 May 8;392(18):1777-1788. doi: 10.1056/NEJMoa2409029. Epub 2024 Dec 9. PMID: 39652675.

With over 30 years of experience in developing and manufacturing high quality ELISA kits we provide scientists and healthcare professionals with tests that enable discoveries and support the translation of research into diagnostics.

All Kits are developed & manufactured by Biomedica Immunoassays – Austrian Quality!

 

Discover our Biomarker ELISA Kit Collection

Trusted and widely cited ELISA assays for biomarkers in bone metabolism, cardiovascular and renal diseases, cancer and oxidative stress.

Biomedica´s ELISA Kits – Features & Benefits

• EASY – ready to use calibrators & controls included (color-coded reagents)
• FULL VALIDATION PACKAGE – assays are optimized for clinical samples following high level international quality standards.
• HIGH QUALITY GUARANTEED – results you can rely on
• WIDELY CITED in over 2500 publications

 

Discover our Biomarker ELISA Kit Collection

BONE 

Sclerostin (SOST), Osteoprotegerin (OPG), Free soluble RANKL (sRANKL), Periostin (POSTN)

Fibroblast Growth Factor (C-terminal and intact) FGF23 intact, FGF23 (C-terminal)

related citations:

• Sclerostin ELISA (BI-20492) : The effect of calcium supplementation on bone calcium balance and calcium and bone metabolism during load carriage in women: a randomized controlled crossover trial. 
• FGF23 ELISAs (BI-20702, BI-20700): C-terminal and intact FGF23 in kidney transplant recipients and their associations with overall graft survival. 

 

CARDIOASCULAR

Natriuretic Peptides: NT-proANP (for human and preclinical use), NT-proBNP, NT-proCNP,                  

Endothelins: Big Endothelin-1 (Big ET-1)

Rat NT-proBNP

• related citation: rat NT-proBNP ELISA (BI-1204R): Leucine Supplementation Improves Diastolic Function in HFpEF by HDAC4 Inhibition.

 

KIDNEY   

Endostatin, Vanin-1

• related citation Vanin-1 ELISA (BI-VAN1U): The Usefulness of Vanin-1 and Periostin as Markers of an Active Autoimmune Process or Renal Fibrosis in Children with IgA Nephropathy and IgA Vasculitis with Nephritis-A Pilot Study. 

 

CANCER

Semaphorin 4D, Neuropilin-1, Leucine-rich alpha-2-glycoprotein (LRG1), Periostin 

• related citation LRG-1 ELISA (BI-LRG): High serum levels of leucine-rich α-2 glycoprotein 1 (LRG-1) are associated with poor survival in patients with early breast cancer. 

 

OXIDATIVE STRESS   

Autoantibodies to oxidized low density lipoprotein (anti-oxLDL AB – oLAB)

OxyStat – detection of biological peroxides

• related citation oxLDL – oLAB ELISA (BI-20032): Novel approaches for the assessment of relative body weight and body fat in diagnosis and treatment of anorexia nervosa: A cross-sectional study.

 

TRANSPLANTATION    

anti-C4D antibody

• related citation anti-C4d Antibody (BI-RC4D): Complement Activation Is Associated With Crescents in IgA Nephropathy. 

 

Biomedica also offers Custom Analytical Service Measurements

• ELISA & LUMINEX
• NEXT-GENERATION SEQUENCING
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“ We have been using the Biomedica ELISA kits for measurements of OPG and soluble RANKL in several contexts and are very pleased with how well they perform both in terms of specificity and reproducibility. For the RANKL kit the measurements are validated by no measurable free soluble RANKL when analyzing culture media where a RANKL inhibitor has been added. Furthermore, we have measured the proteins in a range of human body fluids as well as in tissue and cell culture media and the kits work both when larger and smaller concentrations are measured and when samples are diluted. Martin Blomberg Jensen, MD, DMSc, Andrologist, Dept.Growth and Reproduction 5064, Rigshospitalet, Denmark.”

Example:

“Clinically Relevant Plasma Levels of NT-proBNP in Rats

We are highly satisfied with the results, as we clearly observed clinically relevant levels and the anticipated changes from baseline to completion. Philippa Phelp, Amsterdam UMC”

Review today!

How to write an impactful product review

• Start with a headline – include Product Name and Catologue Number
• Share your experience – add application e.g. we used EDTA-Plasma samples to measure xxx …
• What are the product´s benefits
• Provide honest Pro´s and Con´s of the product
• Include as much information as you wish
• If you have used a similar product before- you could provide a comparison and offer your opinion

Our custom sample testing services are designed to meet the unique needs of your business by providing accurate, reliable, and comprehensive testing solutions tailored to your specific requirements.

What We Offer: 

• Tailored Testing Protocols:  testing procedures customized to your specifications
• Verified Results: comprehensive results presented in an analytical report

• Rapid Turnaround: our flexible testing schedules help you get the results you need promptly, supporting your goals
• Expert Consultation: work with experienced scientists and technicians who understand and can provide valuable insights into biomarker testing

 

Why Choose Our Custom Sample Testing Services?

– Accuracy & Reliability: state-of-the-art equipment and stringent quality control protocols guarantee precise results

– Confidentiality: we prioritize your privacy and proprietary information

– Flexible Solutions: our services are adaptable to your requirements

– Cost-Effective: customized testing plans that maximize value and minimize unnecessary expenditure

 

Partner with us! Tailored solutions for biomarker assessment.

Contact us today to discuss your specific testing needs and experience our dedicated, personalized service (info@bmgrp.com).

Take a look at our workflow diagram

 

Related Literature

An overview of ELISA: a review and update on best laboratory practices for quantifying peptides and proteins in biological fluids. Aydin S, Emre E, Ugur K, Aydin MA, Sahin İ, Cinar V, Akbulut T. J Int Med Res. 2025 Feb;53(2):3000605251315913. doi: 10.1177/03000605251315913. PMID: 39922798; PMCID: PMC11808753.

Abstract

The enzyme-linked immunosorbent assay (ELISA) detects antigen-antibody interactions by using enzyme-labelled conjugates and enzyme substrates that generate colour changes. This review aims to provide an overview of ELISA, its various types, and its applications in detecting metabolites in biological fluids. The article discusses the history of the assay, its underlying principles and procedures, common ELISA protocols, and the most accurate and reliable techniques for measuring peptide molecules in biological fluids. Additionally, we emphasize best laboratory practices to achieve consistent, high-quality results and outline the essential materials for setting up an ELISA laboratory, drawing from our over 30 years of experience in the field.

Comparison between a Luminex-based multiplex kit with a sequence-specific oligonucleotide probe and next-generation sequencing for the detection of POLE oncogenic mutations in endometrial cancer. Kato MK, Kawai T, Okada H, Kondo T, Shiraishi T, Yamaguchi M, Higuchi D, Komatsu M, Hamamoto R, Matumoto K, Terao Y, Kato T, Kohno T, Ishikawa M, Shiraishi K, Yoshida H. Virchows Arch. 2025 Aug 4. doi: 10.1007/s00428-025-04204-4. Epub ahead of print. PMID: 40760194.

We operate in more than 60 countries, providing wide access and customer support through collaborations with carefully chosen local distributors on nearly every continent. No matter where you are, we’re committed to helping you achieve your objectives. With over 30 years of expertise, we focus on designing and manufacturing premium ELISA assay kits for biomarker detection in clinical research.

About us

We develop and produce high-quality ELISA assay kits for clinical and pre-clinical applications related to bone and cardio-renal diseases. Our assays are cited in more than 2500 publications and some of our kits are the most referenced on the market Sclerostin, free soluble RANKL, Periostin, NT-proCNP and many others.

Our ELISA Kits Go Global

All Biomedica ELISA assays undergo a full validation following international quality guidelines (the validation package for every kit can be found on the respective product pages on our website. Validation criteria include recovery, dilution linearity, parallelism, matrix effect testing and many others.

Our ELISA kits include ready-to-use serum-based calibrators and controls enabling researchers to collect biologically reliable data.

 

Features & Benefits of BIOMEDICA ELISA Assay Kits

• Trusted – cited in over 2500 publications
• Highly specific – characterized epitope-mapped antibodies

• Full validation package – following international quality guidelines
• Convenient – ready to use, color coded reagents – controls included 

 

Biomarker ELISA Assays for Bone-Mineral Metabolism & Cardio-Renal Diseases

 –Intact FGF23 ELISA Kit | BI-20700

–FGF23 (C-terminal) multi-matrix ELISA Kit | BI-20702

–Sclerostin ELISA | BI-20492

–FREE soluble RANKL HS ELISA | BI-20462

–Periostin ELISA | BI-20433

–OPG ELISA Kit (Human Osteoprotegerin) | BI-20403

–NT-proBNP ELISA | SK-1204

–Rat NT-proBNP ELISA | BI-1204R

–NT-proANP ELISA | BI-20892

 

Selected citations

Fibroblast Growth Factor 23, Endogenous Erythropoietin, Erythropoiesis-Stimulating Agents, and Erythropoietin Resistance in Hemodialysis Patients.  Hamano N et al.,2025;  Am J Nephrol.

Fibroblast growth factor 23 is associated with the development of gestational diabetes mellitus. Hocher CF et al., 2023; Diabetes Metab Res Rev.

The effect of calcium supplementation on bone calcium balance and calcium and bone metabolism during load carriage in women: a randomised controlled crossover trial. Coombs CV et al., 2025; J Bone Miner Res.  

Bone proteins are associated with cardiovascular risk according to the SCORE2-Diabetes algorithm. González-Salvatierra S et a., 2024; Cardiovasc Diabetol.

 

 

Our proANP ELISA was featured in a recent study investigating the effect of Atrial natriuretic peptide (ANP) in the regulation of endothelial autophagy in human umbilical vein endothelial cells (HUVECs) (1). Autophagy is a lysosome-mediated degradation process vital for cell survival, differentiation, development, and maintaining homeostasis. Its primary function is to act as an adaptive mechanism, helping organisms defend against various conditions such as infections, cancer, neurodegenerative disorders, aging, and cardiovascular diseases (2).

ANP activates autophagy in endothelial cells

ANP is a hormone mainly produced by the atria of the heart, especially in response to increased stretch caused by higher blood volume or pressure. ANP is vital for managing blood volume and pressure by encouraging the excretion of sodium (natriuresis), water (diuresis), and causing blood vessels to dilate (vasodilation) (3). Additionally, it suppresses the renin-angiotensin-aldosterone system (RAAS), which further helps to lower blood pressure. Interestingly, ANP has recently been identified as an extracellular regulator of cardiac autophagy (4).

Atrial natriuretic peptide (ANP) modulates stress-induced autophagy in endothelial cells. Forte M et al., Biochim Biophys Acta Mol Cell Res. 2025 

Key findings:

-ANP quickly enhances autophagy in endothelial cells

-Endothelial cells rapidly secrete ANP under stress conditions promoting stress-induced autophagy

-The protective effects of ANP, such as in response to high-salt conditions, are diminished when autophagy is inhibited

Conclusion: the results suggest that ANP functions as an endogenous activator of autophagy in endothelial cells, with autophagy mediating its protective effects on the endothelium.

NT proANP ELISA | BI-20892

• CONVENIENT – Small sample volume – 10 µl / well
• HIGH QUALITY – Full validation package
• TRUSTED – cited in over 170 publications
• EASY – color coded and ready to use reagents
• FLEXIBLE- assay is suitable for human and non-human samples (rodents and others)

 

 

Related ELISA kits:

NT-proCNP ELISA | BI-20812

NT-proBNP ELISA | SK-1204

Rat NT-proBNP ELISA | BI-1204R

 

Literature:

1. Atrial natriuretic peptide (ANP) modulates stress-induced autophagy in endothelial cells. Forte M, Marchitti S, di Nonno F, Pietrangelo D, Stanzione R, Cotugno M, D’Ambrosio L, D’Amico A, Cammisotto V, Sarto G, Rocco E, Simeone B, Schiavon S, Vecchio D, Carnevale R, Raffa S, Frati G, Volpe M, Sciarretta S, Rubattu S. Biochim Biophys Acta Mol Cell Res. 2025 Jan;1872(1):119860. doi: 10.1016/j.bbamcr. 2024.119860. Epub 2024 Oct 9. PMID: 39383950.
2. Autophagy in the pathogenesis of disease. Levine B, Kroemer G. Cell. 2008 Jan 11;132(1):27-42. doi: 10.1016/j.cell.2007.12.018. PMID: 18191218; PMCID: PMC2696814.
3. Cardiac natriuretic peptides. Goetze JP, Bruneau BG, Ramos HR, Ogawa T, de Bold MK, de Bold AJ. Nat Rev Cardiol. 2020 Nov;17(11):698-717. doi: 10.1038/s41569-020-0381-0. Epub 2020 May 22. PMID: 32444692.
4. NPPA/atrial natriuretic peptide is an extracellular modulator of autophagy in the heart. Forte M, Marchitti S, Di Nonno F, Stanzione R, Schirone L, Cotugno M, Bianchi F, Schiavon S, Raffa S, Ranieri D, Fioriniello S, Della Ragione F, Torrisi MR, Carnevale R, Valenti V, Versaci F, Frati G, Vecchione C, Volpe M, Rubattu S, Sciarretta S.Autophagy. 2023 Apr;19(4):1087-1099. doi: 10.1080/15548627.2022.2115675. Epub 2022 Sep 6. PMID: 35998113; PMCID: PMC10012953.

 

Arterial stiffness (AS) is characterized by stiffening of the vascular wall, which diminishes its ability to expand and contract in response to blood flow. It is a natural aspect of aging, driven by structural and cellular alterations in the vessel walls, and tends to accelerate in the presence of cardiovascular risk factors like diabetes, hypertension, and others (1). The development of AS involves dysregulation of elastin fibers and collagen, oxidative stress, disrupted mineral metabolism, and low-grade inflammation. Multiple factors contribute to its progression, including oxidative stress, inflammation, vascular calcification, and the combined effects of traditional cardiovascular risk factors such as diabetes mellitus and hypertension (2). Arterial stiffness can lead to increased myocardial preload and decreased perfusion pressure in the coronary arteries. Importantly, AS is a predictor of future cardiovascular disease (CVD), as heightened arterial stiffness can cause higher systolic blood pressure, increased cardiac workload, and a greater likelihood of events like heart attack and stroke (3).

Sclerostin is associated with risk for arterial stiffness

Sclerostin is primarily known for its role in controlling bone formation, but it is also expressed in the heart, aorta, and arteries (4). A recent study in community dwelling women revealed that lower serum sclerostin levels were associated with elevated risks for increased AS (5).

Sclerostin levels were measured with the

Biomedica SCLEROSTIN ELISA Assay | BI-20492

• most referenced in over 300 publications
• full validation package
• for serum and plasma – sample volume: 20µl / well

 

 

Example of a typical ELISA assay with color coded, ready to use reagents

Literature:

1. Arterial Stiffness in Aging: Does It Have a Place in Clinical Practice?: Recent Advances in Hypertension. Mitchell GF. Hypertension. 2021 Mar 3;77(3):768-780. doi: 10.1161/HYPERTENSIONAHA.120.14515. Epub 2021 Feb 1. PMID: 33517682..
2. Hypertension, Arterial Stiffness, and Diabetes: a Prospective Cohort Study. Tian X, Zuo Y, Chen S, Zhang Y, Zhang X, Xu Q, Wu S, Wang A. Hypertension. 2022 Jul;79(7):1487-1496. doi: 10.1161/HYPERTENSIONAHA.122.19256. Epub 2022 May 16. PMID: 35574838; PMCID: PMC9172905.
3. Role of arterial stiffness in cardiovascular disease. Cecelja M, Chowienczyk P. JRSM Cardiovasc Dis. 2012 Jul 31;1(4):cvd.2012.012016. doi: 10.1258/cvd.2012.012016. PMID: 24175067; PMCID: PMC3738327.
4. Role of Sclerostin in Cardiovascular Disease. Golledge J, Thanigaimani S. Arterioscler Thromb Vasc Biol. 2022 Jul;42(7):e187-e202. doi: 10.1161/ATVBAHA.122.317635. Epub 2022 May 12. PMID: 35546488.
5. Association of Lower Serum Sclerostin Levels With Elevated Risk for Increased Arterial Stiffness: The JPOS Cohort Study. Tamaki J, Tachiki T, Jaalkhorol M, Dongmei N, Komastu M, Tsuda K, Kudo A, Kamiya K, Kouda K, Kajita E, Kagamimori S, Iki M. J Clin Endocrinol Metab. 2025 Jul 15;110(8):2225-2235. doi: 10.1210/clinem/dgae795. PMID: 39530177.