Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of Alagebrium (ALT-711) and MOTS-c — mechanism, dosing, side effects, legal status, and pricing.
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.
MOTS-c is a 16-amino-acid mitochondrial-derived peptide (MDP) encoded within the mitochondrial 12S rRNA, discovered by Lee and Cohen at USC in 2015 (sequence: MRWQEMGYIFYPRKLR). It is an investigational, research-only peptide studied as a metabolic regulator; it has not been approved by the FDA for any indication.
Alagebrium (ALT-711)
MOTS-c
Category
Legal Status
Mechanism
Dose Range
Route
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
Alagebrium (ALT-711)
MOTS-c
COA corpus from Disclosed Labs — independently tested batches only.
Alagebrium (ALT-711)
2
COAs
99.6%
Avg purity
2
Labs
MOTS-c
193
COAs
99.5%
Avg purity
16
Labs
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.
Lee et al. (Cell Metabolism, 2015; PMID 25738459) identified MOTS-c and showed that exogenous administration in mice prevented diet-induced obesity and insulin resistance via AMPK activation in skeletal muscle. Kim et al. (Cell Metabolism, 2018; PMID 29983246) demonstrated that MOTS-c translocates to the nucleus under metabolic stress and regulates antioxidant response element (ARE) genes. Reynolds et al. (Nature Communications, 2021; PMID 33473109) reported that exercise induces MOTS-c in human skeletal muscle and that MOTS-c treatment improved physical capacity in young, middle-aged, and aged mice. Human clinical data are limited to CohBar's Phase 1a/1b study of the analog CB4211 in healthy volunteers and obese NAFLD subjects, which reported acceptable tolerability and exploratory signals on ALT/AST and glucose; CohBar wound down the program in 2023. No completed Phase 2 or Phase 3 trials exist for MOTS-c or its analogs, and grey-market dosing (typically ~10 mg SubQ 2-3x/week) is not clinically validated.
Alagebrium (ALT-711) and MOTS-c are both in the Metabolic category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
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Key references