SS-31 Reconstitution Calculator

Yes, for one indication. Elamipretide (FORZINITY) received accelerated FDA approval in 2025 as the first treatment indicated specifically for improving muscle strength in Barth syndrome, a rare X-linked mitochondrial cardiomyopathy/myopathy (RCT-backed regulatory approval). No other use (aging, metabolic disease, neuroprotection, or athletic performance) is approved; off-label supplies come from unregulated peptide vendors, and rigorous human safety data for those uses are scarce (observational).

SS-31 is a positively charged tetrapeptide that selectively binds cardiolipin on the inner mitochondrial membrane, stabilizing cristae structure, reducing oxidative stress, and raising ATP production (mechanistic). It also binds the adenine nucleotide translocator (ANT), increasing ADP sensitivity and respiration in aged mitochondria (animal). Human trial programs include PROGRESS-HF, TAZPOWER, MMPOWER-3, and ReCLAIM (RCT).

Subcutaneous. Documented human use is parenteral (subcutaneous); the unmodified peptide is rapidly cleared renally, a pharmacokinetic limitation driving PEGylation/nanoparticle work (animal). One documented human regimen is 10 mg/day SC for 6 months in a 5-year-old Barth patient (case report). Community off-label protocols run 4–10 mg SC daily or every other day (community protocol). Store lyophilized vials frozen (−20°C); after reconstitution, refrigerate and use within ~14–30 days (community protocol).

Not advised. Mitochondrial antioxidants including SS-31 show preclinical potential in gestational diabetes models, but no clinical confirmation of effectiveness during pregnancy exists (animal). Avoid (practitioner consensus).

Barth patients remain on it chronically under the approved indication. In animals, 8 weeks of treatment reversed markers of aortic aging and inflammation in aged mice, and SS-31 given four weeks after surgery rescued memory and hippocampal mitochondrial respiration in aged rats (animal). Community protocols typically cycle 8–12 weeks on, followed by a break (community protocol).

In head-to-head testing in aged MASLD mice, MitoQ (25 mg/kg/day oral) mainly upregulated antioxidant defenses (SOD2, Nrf2), while SS-31 (3 mg/kg/day IP) better preserved mitochondrial structural integrity; both suppressed NF-κB/NLRP3 inflammation, improved insulin signaling, and reduced hepatic steatosis (animal). Practical distinctions: MitoQ is orally bioavailable; SS-31 is injectable with a cardiolipin-binding mechanism.

Yes. SS-31 plus nicotinamide mononucleotide (NMN) outperformed either monotherapy in a mouse ischemic stroke model, suppressing neuroinflammation and apoptosis through the NF-κB/TREM2 axis (animal). Mechanisms are complementary: cardiolipin stabilization vs. NAD+ precursor support. Combined use is common in community protocols (community protocol).

In aged muscle, SS-31 increased ADP sensitivity, improved ATP production, and rescued muscle force, and it improved skeletal muscle performance in a HFpEF rat model (animal). However, human efficacy and safety data for longevity or athletic use are lacking (observational), and in HFpEF myocardium elamipretide improved bioenergetics without translating into measurable functional benefit, a caution against extrapolating from bioenergetic markers (animal). Reported adverse event: one transient asymptomatic pancreatic-enzyme elevation in the pediatric Barth case, resolving without discontinuation (case report). Anti-doping status was not covered in the reviewed evidence; athletes considering SS-31 for performance use should verify the current WADA Prohibited List before use.