Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of Humanin and SS-31 — mechanism, dosing, side effects, legal status, and pricing.
Humanin is a mitochondrial-derived peptide encoded within the 16S ribosomal RNA gene. It was discovered through its ability to protect neurons from Alzheimer's disease-related toxicity and is studied for neuroprotection, metabolic regulation, and anti-aging applications.
SS-31 (elamipretide) is a mitochondria-targeted tetrapeptide (D-Arg-Dmt-Lys-Phe-NH2) developed by Hazel Szeto (Cornell) and clinically advanced by Stealth BioTherapeutics. It concentrates in the inner mitochondrial membrane by binding cardiolipin. In September 2025, the FDA granted accelerated approval to elamipretide (brand name FORZINITY) as the first therapy for Barth syndrome — the first FDA-approved mitochondria-targeted drug. It remains investigational for other indications.
Humanin
SS-31
Category
Legal Status
Mechanism
Dose Range
Route
Frequency
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
Humanin
SS-31
COA corpus from Disclosed Labs — independently tested batches only.
Humanin
3
COAs
99.5%
Avg purity
2
Labs
SS-31
65
COAs
99.8%
Avg purity
12
Labs
Hashimoto et al. (2001) discovered humanin through functional screening for neuroprotective factors against amyloid-beta toxicity. Yen et al. characterized the S14G-Humanin analog (HNG) as 1000x more potent. Muzumdar et al. demonstrated that humanin improves insulin sensitivity and reduces visceral fat in animal models. Circulating humanin levels decline with age and correlate inversely with Alzheimer's biomarkers. Cohen et al. showed humanin's role in the GH/IGF-1 axis through IGFBP-3 interaction. No human clinical trials have been conducted — all dosing is extrapolated from preclinical data.
Key references
The original SS-peptide class was described by Zhao, Szeto and colleagues (J Biol Chem 2004, PMID 15178689), showing ~1000-fold concentration at the inner mitochondrial membrane and protection against oxidative cell death. Szeto's 2014 review (Br J Pharmacol, PMID 24117165) reframed the mechanism as cardiolipin-binding rather than antioxidant scavenging. The TAZPOWER trial (NCT03098797) in Barth syndrome, with its 168-week open-label extension (Thompson et al., Genet Med 2024, PMID 38602181), supported FDA accelerated approval of FORZINITY in September 2025 at 40 mg SubQ daily. The Phase 3 MMPOWER-3 trial in primary mitochondrial myopathy (Karaa et al., Neurology 2023, PMID 37268435) FAILED co-primary endpoints of 6-minute walk test and fatigue score, though a post-hoc nuclear-DNA subgroup showed improvement. Phase 2 ReCLAIM-2 in geographic atrophy missed primary endpoints but reduced ellipsoid-zone attenuation; a Phase 3 trial is ongoing. Earlier heart failure trials (PROGRESS-HF) showed only modest signals.
Key references
Humanin (Cognitive) and SS-31 (Recovery) are in different categories and target different biological pathways. This is a common pattern in multi-compound research protocols. Researchers should monitor the biomarkers from both profiles and watch for interactions listed in each compound’s contraindications. Consult a licensed healthcare provider before combining any research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
Dosing Notes
Half-life
Side Effects
Contraindications
Lab Testing
Disclosed Labs