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Tetrapeptide · cardiolipin-binding · aka elamipretide
A cardiolipin-binding tetrapeptide (D-Arg-Dmt-Lys-Phe), also filed as elamipretide. Supplied as a lyophilized powder for research purposes only.
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Tested lot by lot at ≥99% purity. The Janoshik certificate for your lot is emailed with the order.
Everything Valtrax Research ships is bench material for in-vitro work. None of it is a drug, a supplement, a cosmetic, or a medical device, and none of it is intended for human or animal use, ingestion, or administration. Placing an order is your confirmation that you are a qualified researcher buying for lawful research, under every Canadian law and regulation that applies to you.
Four residues, one alternating cationic–aromatic motif (D-Arg-Dmt-Lys-Phe), and a single trick: the molecule slips across the outer mitochondrial membrane without a transporter and parks on cardiolipin in the inner membrane. SS-31 — also filed as elamipretide — is built around that selectivity, which is why a peptide this small concentrates where it does.
What it binds is the point. Cardiolipin holds the respiratory supercomplexes in shape; when it oxidizes, the cristae loosen and electron transport leaks. Work on the bench uses SS-31 to ask what stabilizing that lipid does to a failing bioenergetic system.
The through-line is cardiolipin. Reports track how SS-31 binding affects inner-membrane structure, respiratory-chain efficiency, and ROS production, then test whether protecting that one lipid changes outcomes in stressed tissue. Recent papers span fibrotic lung, injured skeletal muscle, and cryopreserved cells — different systems, the same mitochondrial premise.
The readout most groups chase is the inner membrane. SS-31 associates with cardiolipin, and the downstream measures follow from that: cristae geometry, supercomplex assembly, ATP output, and the rate at which the electron-transport chain spills reactive oxygen. The peptide is the lever; mitochondrial energetics are the dependent variable.
Sabbah and colleagues have summarized the elamipretide mechanism, and the 2025 literature pushes it into tissue-level questions — pulmonary fibrosis, traumatic muscle injury, sperm cryopreservation — each treating cardiolipin protection as the shared upstream cause.
SS-31 traces to Hazel Szeto and Peter Schiller's work on a series of small, cell-permeant aromatic-cationic peptides — the SS (Szeto-Schiller) series — designed to cross membranes and concentrate in mitochondria without a carrier. The fourth member of that screen became the one that stuck.
Under the clinical name elamipretide it moved into trials for mitochondrial myopathies and heart failure, and that dual identity is why the same compound shows up in the literature under two labels.
Sabbah, H.N. et al. (2025). Contemporary insights into elamipretide’s mitochondrial mechanism of action and therapeutic effects.
PubMedNajafi, A. et al. (2025). Elamipretide enhances post-thaw rooster sperm quality by mitigating oxidative stress and optimizing mitochondrial function during cryopreservation.
PubMedHeo, J. et al. (2025). Acute mitochondrial reactive oxygen species emissions drive mitochondrial dysfunction after traumatic muscle injury in male mice.
PubMedGu, Q. et al. (2025). SS-31: A promising therapeutic agent against bleomycin-induced pulmonary fibrosis in mice.
PubMedIndependent testing lot by lot: identity, purity, net content. The certificate arrives by email with your order.
Janoshik Analytical, a laboratory Valtrax does not own, runs the testing — identity by mass spectrometry, purity by RP-HPLC at ≥99%. The certificate covering the lot you receive is also emailed with your order.
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