GHK-Cu
A tripeptide-copper complex that supports skin regeneration and wound healing.
Naturally occurring in plasma; levels decline with age. Widely used in topical and compounded formulations.
- Routes
- Injection, Topical
- Composition
- 3 aa + Cu²⁺
Recharging the cellular powerhouse
Injection · Prescription
Educational content. This page describes SS-31 (Elamipretide) for informational purposes only and is not medical advice, diagnosis, or treatment. Consult a licensed provider before starting, stopping, or modifying any therapy.
Researched and maintained by the PepHookup team. Regulatory status last verified April 12, 2026.
Protected against inflammation-driven mitochondrial dysfunction and memory impairment in mice, an early-stage finding not yet tested in people.[8]
SS-31, known generically as elamipretide and historically by the development name Bendavia, is a synthetic, water-soluble tetrapeptide (D-Arg-dimethylTyr-Lys-Phe-NH2). Its sequence is engineered to cross cell membranes and accumulate inside mitochondria, the compartments where cells generate most of their energy. It is the first member of a class designed to protect cardiolipin, a signature phospholipid of the inner mitochondrial membrane.
Elamipretide is one of the most clinically advanced mitochondria-targeted compounds. It has been studied in models of aging, heart failure, kidney injury, eye disease, and inherited mitochondrial disorders, and it has moved through human trials up to and including a pivotal phase 3 study. In September 2025 the FDA granted it accelerated approval as Forzinity for Barth syndrome, making it the first FDA-approved mitochondria-targeted therapeutic.
Because it is now an approved prescription drug for a specific rare disease rather than a research-only compound, the version used outside that indication, including for anti-aging or performance goals, remains investigational and is not supported by approval for those uses.
Elamipretide carries a structure that lets it pass through cell membranes and then concentrate steeply within mitochondria, reaching far higher levels on the inner membrane than in the surrounding cytoplasm. There it associates with the inner membrane rather than acting at a classical cell-surface receptor.
Its central target is cardiolipin, the phospholipid that helps organize the electron transport chain into efficient supercomplexes and shapes the folded cristae where energy production happens. Biophysical work shows the peptide binds lipid bilayers and alters their surface charge, which is proposed to be a key part of how it changes membrane behavior.
By interacting with cardiolipin, elamipretide is thought to preserve cristae architecture, support electron transport efficiency, and limit the conditions under which cytochrome c turns toxic. The downstream effects reported across models are higher ATP output, lower mitochondrial reactive oxygen species, and a restored redox balance, with the largest benefits seen in tissues that already have mitochondrial dysfunction.
Recharging the cellular powerhouse
Elamipretide accumulates on the inner mitochondrial membrane and binds cardiolipin, the lipid that organizes the electron transport chain and shapes cristae. By stabilizing cardiolipin and the membranes around it, the peptide is proposed to preserve cristae structure, support electron transport efficiency, raise ATP output, and reduce reactive oxygen species at their source rather than scavenging them after the fact.
A single intravenous infusion measurably increased in vivo skeletal muscle ATP production capacity compared with placebo, providing early human evidence of a bioenergetic effect.
Roshanravan B, Liu SZ, Ali AS, et al. · PLoS One, 16(7):e0253849 (2021) · PubMed
The placebo-controlled crossover did not meet its primary endpoints, but the open-label extension was the basis for later approval data. This was the pivotal program for the eventual FDA accelerated approval.
Reid Thompson W, Hornby B, Manuel R, et al. · Genet Med, 23(3):471-478 (2021) · PubMed
Over up to 168 weeks, knee extensor muscle strength and six-minute walk distance improved relative to study baseline, with injection site reactions the most common adverse event. These data supported the 2025 accelerated approval.
Thompson WR, Manuel R, Abbruscato A, et al. · Genet Med, 26(7):101138 (2024) · PubMed
A single infusion was safe and well tolerated. The highest dose was associated with significant reductions in left ventricular end-diastolic and end-systolic volumes, an early signal that did not translate into approval for heart failure.
Daubert MA, Yow E, Dunn G, et al. · Circ Heart Fail, 10(12):e004389 (2017) · PubMed
Higher doses were associated with improvement in six-minute walk distance, supporting progression to a larger phase 3 trial.
Karaa A, Haas R, Goldstein A, et al. · Neurology, 90(14):e1212-e1221 (2018) · PubMed
Well tolerated but did not meet its primary endpoints over 24 weeks, underscoring how difficult it is to reverse established, genetically driven mitochondrial disease.
Karaa A, Bertini E, Carelli V, et al. · Neurology, 101(3):e238-e252 (2023) · PubMed
Daily subcutaneous dosing was generally well tolerated, with exploratory visual function signals that motivated further eye-disease research. This is hypothesis-generating, not confirmatory.
Allingham MJ, Mettu PS, Cousins SW · Ophthalmol Sci, 2(1):100095 (2022) · PubMed
start low, go slow
Subcutaneous Injection
Intravenous Infusion
Subcutaneous Injection: Forzinity is approved for Barth syndrome in patients weighing at least 30 kg. Dosing for any use is determined by a licensed provider.
Intravenous Infusion: The IV route was used in heart failure and single-dose ATP studies and is not a take-home protocol.
Dosing should always be determined by a licensed provider based on the condition being treated, body weight, and clinical goals. The only dose with regulatory backing is the 40 mg daily subcutaneous regimen for Barth syndrome.
Mitochondrial uptake is rapid, and a single dose produced measurable changes in human muscle ATP within hours in one study, but rapid uptake does not mean rapid symptom relief.
Outside of approved Barth syndrome use, elamipretide remains investigational, and there is no established consumer anti-aging or performance protocol supported by trial data.
Across multiple trials, including the 218-patient phase 3 MMPOWER-3 study over 24 weeks, most adverse events were mild to moderate, and injection site reactions were the dominant finding. The Barth syndrome program reported a consistent safety profile over long-term open-label dosing.
Effects in studies were most pronounced in aged or diseased tissue. There is little evidence it meaningfully changes mitochondrial function in young, healthy tissue, which tempers expectations for general anti-aging or performance use.
Long-term safety data outside the narrow Barth syndrome population are limited, and self-directed use of research-grade material carries additional purity and dosing risks that an approved, pharmacy-dispensed product does not.
| Peptide | Primary Use | Administration | Cycle Length | Key Differentiator |
|---|---|---|---|---|
| SS-31 (Elamipretide) | Mitochondrial restoration and rare mitochondrial disease | Subcutaneous injection (daily); IV in trials | Ongoing daily dosing | The first FDA-approved mitochondria-targeted therapeutic; binds cardiolipin on the inner mitochondrial membrane to support electron transport efficiency |
| GHK-Cu | Anti-Aging & Skin Regeneration | Topical, Injection | 8-12 weeks | A naturally occurring copper-carrier peptide that rebuilds the skin matrix and, per gene-expression analysis, shifts expression of about a third of human genes toward repair |
| Sermorelin | GH restoration and healthy aging | Subcutaneous injection, daily at bedtime | 3-6 months | The GHRH analog with prior FDA approval and a multi-decade clinical record, preserving natural feedback rather than replacing growth hormone |
| Glutathione | Antioxidant & Detoxification | IV, Oral, Sublingual, Topical | Ongoing supplementation | The body's own master antioxidant, with controlled human data showing oral and sublingual forms can raise body stores and immune markers |
| CJC-1295 | Anti-Aging & Recovery | Subcutaneous injection (weekly with DAC, daily without) | 8-12 weeks | The only GHRH analog with a covalent albumin-binding Drug Affinity Complex, extending its half-life to 6-8 days for once-weekly dosing |
This peptide is an FDA-approved drug available via standard prescription.
FDA-approved as Forzinity for Barth syndrome (mitochondrial disease). First FDA-approved mitochondria-targeted therapeutic. Subcutaneous daily injection for patients weighing at least 30 kg.
FDA granted accelerated approval to Forzinity (elamipretide) injection for Barth syndrome
Last verified April 12, 2026. PepHookup tracks public FDA actions. This is not legal or medical advice.
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Find a ProviderA tripeptide-copper complex that supports skin regeneration and wound healing.
Naturally occurring in plasma; levels decline with age. Widely used in topical and compounded formulations.
A 29-residue GHRH analog that prompts the pituitary to release endogenous growth hormone.
Formerly marketed as Geref for pediatric GH deficiency; discontinued in 2008 for commercial reasons.
A tripeptide antioxidant central to cellular redox, detoxification, and immune function.
Produced endogenously and supplemented via IV, injection, or oral routes; clinical evidence remains mixed.
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