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MOTS-c

Animal studies only

A mitochondria-encoded peptide that acts as a metabolic signal to the rest of the body, studied for insulin sensitivity and exercise capacity.

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SS-31

Early human data

A cardiolipin-targeting peptide that concentrates in the inner mitochondrial membrane, in human trials for primary mitochondrial disease.

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At a glance

At a glance compared across MOTS-c, SS-31
Attribute	MOTS-c	SS-31
Primary use	Mitochondria & energy	Mitochondria & energy
Evidence gradediffers	Animal studies only	Early human data
Human data	No human citations on file	No human citations on file
Cited sources	2 sources · 0 human	2 sources · 0 human
In one sentence	A mitochondria-encoded peptide that acts as a metabolic signal to the rest of the body, studied for insulin sensitivity and exercise capacity.	A cardiolipin-targeting peptide that concentrates in the inner mitochondrial membrane, in human trials for primary mitochondrial disease.

Mechanism

Mechanism compared across MOTS-c, SS-31
Attribute	MOTS-c	SS-31
How it is thought to work	MOTS-c is encoded not in the nucleus but in mitochondrial DNA — one of a small family of peptides that let mitochondria signal outward to the cell and the organism. It activates AMPK, shifts folate-methionine metabolism, and can translocate to the nucleus under metabolic stress to regulate stress-adaptive genes. Its levels decline with age.	SS-31 selectively binds cardiolipin, a phospholipid found almost exclusively in the inner mitochondrial membrane. By stabilising cardiolipin it improves the efficiency of the electron transport chain, reduces electron leak and therefore reactive oxygen species production. It concentrates in mitochondria at roughly a thousand-fold over cytosolic levels.
What the research reports	Improved insulin sensitivity and prevented diet-induced obesity in mice Increased exercise capacity in aged mice Higher circulating levels associated with metabolic health in human observational data AMPK activation, the same pathway targeted by metformin and exercise	Phase 2 and 3 trials in primary mitochondrial myopathy and Barth syndrome Improved mitochondrial respiration and reduced oxidative stress in multiple tissue models Studied in heart failure, ischaemia-reperfusion injury and dry age-related macular degeneration Neuroprotection in animal models of neurodegeneration
What it is NOT shown to do	No completed randomised human trial of exogenous MOTS-c No demonstrated effect on mood or cognition in humans The mood connection is entirely inferential, via the mitochondrial theory of depression	Primary endpoints have been missed in several late-stage trials No approval to date No trial in depression or cognition

Dosing & pharmacology

Dosing & pharmacology compared across MOTS-c, SS-31
Attribute	MOTS-c	SS-31
Routes studied	Subcutaneous	Subcutaneous
Half-lifediffers	Short in circulation; not well characterised in humans	Roughly 2–4 hours in plasma; tissue mitochondrial retention is far longer
Dose reference	No established human dose. Animal studies use weight-scaled amounts that do not translate directly.	Clinical trials used approximately 40 mg/day subcutaneously in adults, under supervision.
Typical study cyclediffers	Not established	Trials ran continuous daily dosing over weeks to months

Chemistry & handling

Chemistry & handling compared across MOTS-c, SS-31
Attribute	MOTS-c	SS-31
Sequence	Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Ala (MRWQEMGYIFYPRKLA)	D-Arg-Dmt-Lys-Phe-NH2 (elamipretide)
Molecular formuladiffers	C101H152N28O22S2	C32H49N9O5
Molecular weightdiffers	≈2174.6 g/mol	639.8 g/mol
CAS numberdiffers	1627580-64-6	736992-21-5
Storage (reconstituted)	2–8 °C, typically used within 2–4 weeks	2–8 °C, typically used within 2–4 weeks

Risk

Risk compared across MOTS-c, SS-31
Attribute	MOTS-c	SS-31
Reported side effects	Injection-site reaction Otherwise uncharacterised in humans	Injection-site reactions — common and frequently the dose-limiting issue Headache Nausea
Contraindications	Pregnancy and breastfeeding Diabetes managed with insulin or sulfonylureas — an AMPK activator can compound hypoglycaemia risk	Pregnancy and breastfeeding Not established outside trial settings