Latest studies
Every paper our editors flag with a plain-language note and an evidence rating. Filter by evidence, species, or design to find what actually applies to you.
- Study · SS-31Weak / none
Breaking a mitochondrial danger-STING feed-forward amplifier preserves alveolar-capillary architecture and dampens interferon-chemokine signaling in acute lung injury.
This preclinical mouse study directly administered elamipretide (SS-31) and reported associations with improved oxidative-stress markers and reduced mitochondrial DNA leak in acute lung injury. SS-31 is a genuine intervention arm here, though the strongest effects came from its combination with a separate STING inhibitor, making its isolated contribution partial. As early animal work, the evidence is preliminary but the peptide is a real subject of the study.
Tissue & celln=—AnimalAug 1, 2026 - Study · SS-31Weak / none
Mitochondrial-targeted SS-31 peptide attenuates radiation-induced cardiomyocyte senescence.
A cell-culture study in which SS-31 was the direct intervention and showed a consistent signal against radiation-induced senescence markers. Findings are mechanistic and preclinical, not evidence of clinical benefit in people.
Journal of radiation researchn=—In vitroJul 15, 2026 - Study · SS-31Supported
Elamipretide: a mitochondria-targeting drug for Barth syndrome.
This review covers elamipretide (SS-31) for Barth syndrome, a use recently supported by regulatory approval. As a brief review it summarizes rather than generates evidence, but it centers a tracked peptide with a clear clinical narrative. Supports a measured, non-promotional writeup noting the ultra-rare indication.
Trends in pharmacological sciencesn=——Jul 14, 2026 - Study · SS-31Weak / none
Elamipretide in pediatric Barth syndrome: from heart failure to school return.
A single pediatric case report of elamipretide (SS-31) in Barth syndrome, with notable improvement alongside maximal standard therapy. As an uncontrolled n-of-1 report it cannot establish causation and one transient adverse event was noted. Carefully framed as a single-patient observation.
Orphanet journal of rare diseasesn=—HumanJul 7, 2026 - Study · SS-31Weak / none
Targeting Mitochondrial Dysfunction With Elamipretide (SS-31) Improves Skeletal Muscle Performance in a HFpEF Rat Model.
A controlled rat study showing SS-31 improving skeletal-muscle function in a HFpEF model, with a plausible cardiolipin-stabilization mechanism. Evidence remains preclinical and animal-only.
Circulation. Heart failuren=—AnimalJun 15, 2026 - Study · SS-31Weak / none
Therapeutic Peptide SS-31 Modulates Membrane Binding and Aggregation of α-Synuclein and Restores Impaired Mitochondrial Function.
A laboratory study using cell cultures and biochemical assays, not human data. SS-31 has been studied for its effects on mitochondrial function and protein aggregation relevant to Parkinson's-type pathology. Findings are early-stage and warrant further preclinical work.
Chemical biology & drug designn=—In vitroJun 1, 2026 - Study · SS-31Weak / none
Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries and Athletic Performance.
This narrative review in Sports Medicine surveys the pharmacological profiles, regulatory standing, and safety data for eleven peptides marketed to athletes and patients seeking injury recovery — ranging from FDA-approved tesamorelin to unapproved compounds such as BPC-157, TB-500, and MOTS-c. The authors' central finding is that a substantial regulatory gap exists: while some peptides (tesamorelin, sermorelin historically) have cleared rigorous approval processes for specific indications, many others circulate in a gray market supported primarily by animal-model data and amplified by social media. A narrative review design is worth flagging. Unlike a systematic review or meta-analysis, it does not involve exhaustive literature search protocols or pooled effect-size estimates, which means it reflects editorial judgment about which evidence to emphasise. That is appropriate for a broad landscape survey but limits the precision of any efficacy conclusions. The key caveat — which the authors acknowledge directly — is that favorable preclinical signals in rodent tissue-repair and metabolic models do not reliably translate to human outcomes. The review also raises an...
Sports medicine (Auckland, N.Z.)n=——Apr 12, 2026 - Study · SS-31Weak / none
Restoring cardiolipin homeostasis mitigates cerebral ischemia-reperfusion injury by suppressing ATG5-mediated neuronal autophagy-dependent ferroptosis.
An animal and cell study in which SS-31 is a central intervention for preserving cardiolipin after ischemia-reperfusion. Evidence is preclinical and mechanistic. A solid data point for SS-31 in stroke research.
Journal of advanced researchn=—AnimalMar 12, 2026 - Study · SS-31Weak / none
Mechanisms of Anti-Oxidants, N-Acetylcysteine and Elamipretide (SS-31), on Ozone-Induced Airway Hyperresponsiveness and Mucus Hypersecretion.
An animal and cell study directly comparing SS-31 and N-acetylcysteine in ozone-induced airway injury, with SS-31 as a primary intervention. Findings are preclinical and mechanistic, not evidence of human benefit.
Lungn=—AnimalMar 9, 2026 - Study · SS-31Supported
2025 FDA TIDES (Peptides and Oligonucleotides) Harvest.
A review of 2025 FDA peptide and oligonucleotide approvals that documents elamipretide's approval for Barth syndrome, a specific inherited condition. A notable regulatory milestone for the peptide, though the approval is narrow and disease-specific. Useful context for SS-31 coverage.
Pharmaceuticals (Basel, Switzerland)n=——Jan 30, 2026 - Study · SS-31Weak / none
SS-31 improves the quality of maternally aged oocytes by ameliorating mitochondrial function and metabolism.
An animal study in aged mice using SS-31 as the primary intervention for oocyte quality. Findings are preclinical and associative, not applicable to human fertility. A solid SS-31 data point in reproductive aging.
Journal of ovarian researchn=—AnimalJan 29, 2026 - Study · SS-31Contradicted
Mitochondrial Targeting by Elamipretide Improves Myocardial Bioenergetics Without Translating into Functional Benefits in HFpEF.
An animal study in obese ZSF1 rats where elamipretide improved mitochondrial respiration but did not translate into functional or structural cardiac improvement, and systolic performance modestly declined. A notable negative finding for the peptide in established HFpEF, a valuable counterweight to more optimistic preclinical reports.
International journal of molecular sciencesn=—AnimalJan 21, 2026 - Study · SS-31Weak / none
Elamipretide Improves Mitochondrial Function in Mitochondrial Trifunctional Protein-Deficient Mice and Human Fibroblasts.
A preclinical study testing elamipretide (SS-31) directly in a mouse model and human fibroblasts of trifunctional protein deficiency, reporting improved endurance and mitochondrial enzyme activity though cardiolipin content was unchanged. Framed as a candidate warranting further work, not an established therapy.
Journal of inherited metabolic diseasen=—AnimalJan 1, 2026 - Study · SS-31Weak / none
Elamipretide (SS-31) promotes recovery by preserving mitochondrial bioenergetics and neural remodeling after spinal cord injury.
An animal study in mice with supporting cell-culture work; SS-31 is the primary intervention. Results are associative and preclinical, not evidence of benefit in humans. A reasonable data point for tracking SS-31 in neural-injury research.
Neurochemistry internationaln=—AnimalJan 1, 2026