Alagebrium (ALT-711)

Overview

Alagebrium (ALT-711) is a thiazolium-derived non-peptide small molecule investigated as an advanced glycation end-product (AGE) crosslink breaker. It reached Phase I–III human trials (2001–2010) for diastolic heart failure and hypertension but was never approved; clinical development was discontinued around 2009 due to financial constraints. No validated human dose exists. Currently sold by research-chemical vendors for research use only.

Mechanism of Action

Proposed to chemically cleave alpha-dicarbonyl carbon–carbon bonds within certain advanced glycation end-product (AGE) protein crosslinks, releasing crosslinked collagen and proteins in vascular and myocardial tissue and thereby reducing tissue stiffness. Additional proposed activities include methylglyoxal scavenging and metal chelation (e.g., inhibition of copper-catalyzed ascorbate oxidation); whether in vivo effects arise from AGE-crosslink cleavage versus metal chelation is unresolved. There is no evidence it cleaves glucosepane, considered the most abundant AGE crosslink in human tissue, which limits confidence in crosslink-breaking as the sole explanation for observed effects.

Research Summary

Alagebrium reached Phase I–III human trials (2001–2010) under sponsor Alteon Inc./Synvista Therapeutics but was never approved. A 16-week open-label pilot in 23 elderly patients (21 completers) with diastolic heart failure showed reduced left ventricular mass and improved Doppler diastolic index (E') without change in blood pressure, ejection fraction, or exercise capacity. The SPECTRA trial (ALT-711 + hydrochlorothiazide in hypertension) was terminated; the BENEFICIAL trial (chronic heart failure) was completed but did not meet efficacy endpoints. Preclinical studies in non-diabetic hypertensive rats, aged dogs, aged monkeys, streptozotocin-induced diabetic rats, and diabetic mouse models demonstrated improved vascular/cardiac function, reduced aortic stiffness, decreased collagen crosslinking, and improved renal pathology. A 2-year rat toxicology study found liver alterations that prompted a temporary enrollment suspension pending review.

Vendors selling Alagebrium (ALT-711)

Scored vendors carrying Alagebrium (ALT-711), ranked by trust grade. Grades are computed from indexed Certificates of Analysis. Full $/mg pricing is on the comparison page.

Reported Side Effects

• Small number of gastrointestinal symptoms (elderly diastolic heart failure pilot)
• Liver alterations in 2-year rat toxicology study (animal finding, not confirmed human hepatotoxicity)
• No deaths or notable side effects in Phase I trials
• No FDA/EMA-reviewed human safety database (drug never approved)
• WADA doping status unconfirmed

Compare Alagebrium (ALT-711) with Others

Research References

• The effect of alagebrium chloride (ALT-711), a novel glucose cross-link breaker, in the treatment of elderly patients with diastolic heart failure. 2005. PMID 15812746.
• Alagebrium and Complications of Diabetes Mellitus (review; Toprak C, Yigitaslan S, Eurasian J Med 2019;51(3):285-292). 2019.
• Functional Effects of Alagebrium (ALT-711) - Isolated Rat Carotid Artery.
• BENEFICIAL: Efficacy and Safety of Alagebrium (ALT-711) in Patients With Chronic Heart Failure (NCT00516646) — status Completed.

Frequently asked questions

Has Alagebrium (ALT-711) been independently lab-tested?

Disclosed Labs has collected 2 Certificates of Analysis (COA) for Alagebrium (ALT-711) from 2 independent testing labs. 1 vendor has submitted material for testing. Products average 99.6% tested purity across the corpus. Full testing data is available at https://www.disclosedlabs.com/peptides/alagebrium/testing.

Where can researchers source Alagebrium (ALT-711)?

1 vendor with Disclosed Labs trust grades currently list Alagebrium (ALT-711), including Kimera Chems. Compare live prices and lab-verified COAs at https://www.disclosedlabs.com/prices/alagebrium.

How does Alagebrium (ALT-711) work?

Proposed to chemically cleave alpha-dicarbonyl carbon–carbon bonds within certain advanced glycation end-product (AGE) protein crosslinks, releasing crosslinked collagen and proteins in vascular and myocardial tissue and thereby reducing tissue stiffness. Additional proposed activities include methylglyoxal scavenging and metal chelation (e.g., inhibition of copper-catalyzed ascorbate oxidation); whether in vivo effects arise from AGE-crosslink cleavage versus metal chelation is unresolved. There is no evidence it cleaves glucosepane, considered the most abundant AGE crosslink in human tissue, which limits confidence in crosslink-breaking as the sole explanation for observed effects.

What does the research say about Alagebrium (ALT-711)?

Alagebrium reached Phase I–III human trials (2001–2010) under sponsor Alteon Inc./Synvista Therapeutics but was never approved. A 16-week open-label pilot in 23 elderly patients (21 completers) with diastolic heart failure showed reduced left ventricular mass and improved Doppler diastolic index (E') without change in blood pressure, ejection fraction, or exercise capacity. The SPECTRA trial (ALT-711 + hydrochlorothiazide in hypertension) was terminated; the BENEFICIAL trial (chronic heart failure) was completed but did not meet efficacy endpoints. Preclinical studies in non-diabetic hypertensive rats, aged dogs, aged monkeys, streptozotocin-induced diabetic rats, and diabetic mouse models demonstrated improved vascular/cardiac function, reduced aortic stiffness, decreased collagen crosslinking, and improved renal pathology. A 2-year rat toxicology study found liver alterations that prompted a temporary enrollment suspension pending review.