SS-31

Chemical Makeup:

• Molecular Formula: C32, H49, N9, O5
• Molecular Weight: 639.8 g/mol
• Synonyms: Elamipretide, MTP-131, Bendavia, D-Arg-Dmt-Lys-Phe-NH2

Sequence:

• D-Arg-Dmt-Lys-Phe-NH2

[SS-31] and Mitochondrial Bioenergetics

Research into [SS-31] focuses heavily on its ability to restore bioenergetics in dysfunctional mitochondria. In experimental models, the peptide has been shown to prevent the oxidation of cardiolipin by cytochrome c peroxidase. Studies suggest that by preserving cardiolipin integrity, [SS-31] prevents the opening of the mitochondrial permeability transition pore (mPTP) and the subsequent collapse of the mitochondrial membrane potential. This mechanism is currently under investigation for its potential to protect cells during metabolic stress.

[SS-31] and Cardiac Function

In murine models of pressure-overload-induced heart failure, administration of [SS-31] was observed to ameliorate left ventricular hypertrophy and preserve systolic function. Investigators noted that the peptide significantly reduced myocardial fibrosis and lung congestion in treated subjects compared to controls. The data indicates that [SS-31] may influence mitochondrial respiration in cardiomyocytes, potentially limiting the maladaptive remodeling processes associated with cardiac stress.

[SS-31] and Neuroprotection

Academic interest extends to the peptide’s effects on neurodegenerative pathways. In rodent models of isoflurane-induced neurotoxicity, pretreatment with [SS-31] was associated with a reduction in reactive oxygen species accumulation in the hippocampus. Furthermore, studies utilizing models of Alzheimer’s disease have reported that the peptide may mitigate mitochondrial fragmentation and improve synaptic viability. These findings suggest a potential influence on cognitive outcomes linked to mitochondrial health, though mechanisms remain a subject of active research.

[SS-31] and Renal Ischemia

The protective effects of [SS-31] have been extensively studied in the context of ischemia-reperfusion (I/R) injury. In renal injury models, the peptide was observed to accelerate the recovery of ATP levels and protect tubular barrier function. Research indicates that [SS-31] concentrates in the kidney rapidly following administration, where it may preserve mitochondrial cristae architecture during ischemic events, thereby reducing subsequent tissue damage.

[SS-31] and Aging (Sarcopenia)

Investigations into age-related muscle decline (sarcopenia) have utilized [SS-31] to explore redox homeostasis. In aged mice, treatment with the peptide was shown to reverse the age-related decline in maximum mitochondrial ATP production (ATP Max) in skeletal muscle. Researchers observed that the peptide reduced oxidative stress markers and improved exercise tolerance in older subjects without altering mitochondrial protein content, suggesting an enhancement of intrinsic mitochondrial quality rather than biogenesis.

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Adverse Events in Animal Studies:

In preclinical toxicology studies involving animal models, [SS-31] has generally been well-tolerated at therapeutic dosages. Documented side effects in murine subjects are typically mild and transient, primarily limited to injection site reactions such as irritation or redness. High-dose studies have monitored for systemic toxicity, with no significant organ dysfunction reported in standard rodent panels. However, long-term safety profiles in non-human primates and other species continue to be evaluated.

Research Use Only:

This product is intended exclusively for laboratory research and development purposes. It is not intended for human consumption, diagnostic use, or therapeutic application. The physiological properties and effects described above are based on academic research and animal studies; they have not been validated by regulatory bodies for use in humans.