SS-31 news and clinical trials

Researchers published a study showing that the peptide elamipretide reduced cisplatin-induced ovarian failure in a mouse model. The treatment preserved mitochondrial function and increased the number of follicles by activating the Nrf2/HO-1 signaling pathway.

Researchers published a study demonstrating that elamipretide improves oocyte quality and fertility in aged mice, human, and porcine models. The peptide restores ovarian function by activating the VEGF signaling pathway to enhance mitochondrial metabolism and organelle organization.

A study in aged mice with metabolic dysfunction-associated steatotic liver disease found that both MitoQ and SS-31 improved liver health, with MitoQ enhancing antioxidant defenses and SS-31 preserving mitochondrial structural integrity.

The Food and Drug Administration announced the renewal of the Cardiovascular and Renal Drugs Advisory Committee. This committee is extended for an additional 2 years, with the new charter remaining in effect until August 27, 2028.

A study found that treatment with 1 µM of SS-31 attenuated senescence markers, mitochondrial ROS production, and mitochondrial respiration elevation in cardiomyocytes treated with 50 nM doxorubicin.

Researchers found that treatment with 1 µM of SS-31 attenuated radiation-induced senescence in cardiomyoblast cells and stem cell-derived cardiomyocytes by mitigating reactive oxygen species and reducing senescence markers.

Researchers published an article regarding elamipretide as a potential mitochondria-targeting treatment for Barth syndrome.

A study in mice found that combining elamipretide and nicotinamide mononucleotide significantly reduced post-ischemic brain damage and neurological deficits compared to either treatment alone by inhibiting the NF-κB/TREM2 signaling axis.

A case report describes a 5-year-old child with Barth syndrome who experienced improvements in cardiac function, nutrition, and quality of life after receiving subcutaneous elamipretide treatment.

A study in heart failure rats found that elamipretide improved skeletal muscle contractile function, prevented muscle atrophy, and increased titin phosphorylation by stabilizing cardiolipin levels in muscle tissue.

A review article summarizes how cardiolipin biosynthesis and remodelling influence mitochondrial health and disease. It evaluates clinical evidence for cardiolipin-targeting stabilizers like Elamipretide and discusses using the MLCL:CL ratio as a lipid biomarker for diagnosis.

Researchers published a study demonstrating that the peptide SS-31 (Elamipretide) displaces alpha-synuclein from cell membranes and inhibits its aggregation in vitro. By hindering cellular uptake of alpha-synuclein oligomers, SS-31 enhanced cell viability and restored mitochondrial function.

A study in a mouse model of spinal cord injury found that elamipretide promoted recovery and improved locomotor performance by mitigating early apoptotic injury and supporting mitochondrial homeostasis.

Stealth BioTherapeutics Inc. registered a Phase 3b/4 clinical trial to evaluate the efficacy and safety of elamipretide in 48 patients with Barth syndrome. The study aims to confirm findings related to improved knee extensor muscle strength.

A study showed that Elamipretide (SS-31) and N-acetylcysteine protect mice from ozone-induced airway injury. Both treatments attenuated airway hyperresponsiveness and mucus hypersecretion by reducing oxidative stress and suppressing PI3K/AKT and inflammatory pathways.

Researchers found that SS-31 supplementation improved oocyte maturation and early embryonic development in aged mice. The peptide restored mitochondrial function and mitophagy while reducing ROS accumulation, DNA damage, and aneuploidy in aged oocytes.

A study in a rodent model of heart failure with preserved ejection fraction (HFpEF) showed that Elamipretide treatment improved mitochondrial respiration but failed to provide functional or structural benefits. The findings suggest limited efficacy once HFpEF is established.

Researchers found that elamipretide improved exercise endurance in βTFP-deficient mice and increased mitochondrial bioenergetics in patient-derived fibroblasts. The peptide shows potential for treating mitochondrial trifunctional protein deficiency.

The Food and Drug Administration issued a priority review voucher to Stealth BioTherapeutics Inc. The agency awarded this voucher because the company's product, FORZINITY (elamipretide), met the established criteria for a rare pediatric disease product application approved on September 19, 2025.

The Children's Hospital of Philadelphia completed an investigator-initiated study involving 20 participants to evaluate the safety, tolerability, and efficacy of elamipretide. The trial focused on treating vision loss associated with Friedreich Ataxia.

David Marcinek registered a Phase 2a pilot study to evaluate the safety and tolerability of daily subcutaneous injections of elamipretide in 30 older adults. This open-label study involves a 4-week intervention period to assess effects on healthy aging and physical function.

The FDA granted accelerated approval to Elamipretide (Forzinity) in September 2025 for treating muscle strength in adult and pediatric Barth syndrome patients weighing >= 30 kg. It is the first disease-specific treatment approved for this rare genetic disorder.

The FDA granted accelerated approval to Elamipretide on September 19, 2025, as a therapy for Barth syndrome. While a clinical trial showed no significant improvement in the 6-minute walk test, patients experienced sustained benefits during a 168-week open-label extension.

SS-31 pretreatment attenuated endothelial glycocalyx degradation and reduced neuroinflammation in aged rats. This indicates the peptide may help prevent cognitive decline linked to systemic inflammation.

This journal article provides information on Elamipretide Hydrochloride. No abstract is available for this entry.

An editorial in Clinical therapeutics discusses the drug FORZINITY, also known as elamipritide.

SS-31 treatment improved survival rates and reduced neurological deficits in a rat model of cardiac arrest. The peptide protected against brain injury by inhibiting microglial ferroptosis through the Sesn2 signaling pathway.