MOTS-c
Also known as: Mitochondrial Open reading frame of the Twelve S rRNA type-c
MOTS-c is an investigational mitochondrial-derived peptide studied preclinically for metabolic regulation. It is research-only and not FDA-approved; the CB4211 analog program (CohBar) was discontinued in 2023.
Pricing for MOTS-c
Live vendor pricing, normalized to $/mg so sizes compare fairly — fused with each seller's Merit trust score and latest independent COA purity. Prices refresh daily.
COAs for MOTS-c
156 third-party tests across 30 vendors. Each card links to the full report.
For
MOTS-C
by Verified Peptides· batch M005261320L
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MOTS-C
by Crush Research· batch CRMTS-40-2605-2
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MOTS-C
by Crush Research· batch CR-MOTS20-2605-1
For
MOTS-C
by Crush Research· batch CRMTS-40-2605-1
For
MOTS-C
by Crush Research· batch CRMTS-10-2605-1
For
MOTS-C
by Nox Amino· batch NA-MS0226-01
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MOTS-C
by NG Peptide· batch MTS40-07
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MOTS-c
by Peptide Supply Co.· batch MC1005192026
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MOTS-c
by Ion Peptide· batch MC10-05072026
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MOTS-c
by Prime Peptides· batch 4052026MO
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MOTS-c
by BioLongevity Labs· batch 18-3-46154
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MOTS-C
by Sunrise Bioresearch· batch MTC10MAY26-01
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MOTS-c
by Crush Research· batch CR-MTS10-0309-1
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MOTS-C
by Ion Peptide· batch MC10-05042026
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Mots-C
by BioLongevity Labs· batch 18-3-46145
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MOTS-c
by BioLongevity Labs· batch 18-3-46136
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MOTS-c
by HongDa Peptide· batch 4
For
MOTS-c
by Verified Peptides· batch M004261220K
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MOTS-C
by Reta Peptide· batch 20260409
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MOTS-c
by OROS Research· batch OR-LPMOTS10-426-B7
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MOTS-c
by Peptide Supply Co.· batch MC1004092026
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MOTS-c
by Qihang Peptide· batch 4
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MOTS-c
by Ion Peptide· batch MC10-04042026
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MOTS-c
by Glacier Aminos· batch MOT20GA-04
24 citations indexed for MOTS-c
animal · 2026
LAT1-mediated delivery of engineered R13A-MOTS-c attenuates radiation-induced lung injury via Nrf2 activation and mitochondrial protection
MOTS-c exhibits substantial antioxidant and anti-inflammatory properties, yet its therapeutic potential is constrained by poor membrane permeability due to its high polarity.
animal · 2026
MOTS-c attenuates hyperoxia-induced neonatal cardiac injury by inhibiting oxeiptosis via maintaining the KEAP1-PGAM5 interaction
Aims Hyperoxia-induced oxidative stress is a primary cause of neonatal injury. Neonatal heart shows a particular susceptibility to hyperoxic toxicity, yet mechanisms and effective therapeutic strategies remain limited. Oxeiptosis is a ROS-specific programmed cell death.
animal · 2026
MOTS-c, a mitochondrial-derived peptide, ameliorates lysosomal membrane permeability and improves survival of soft tissue transplantation
Distal ischemic necrosis remains a major challenge in reconstructive surgery. Mitochondria and lysosomes interact via signaling and membrane contacts to maintain cellular homeostasis.
Study · 2026
Humanin and MOTS-c Attenuate Atrial Fibrillation by Suppressing Fibrosis and Mitochondrial Dysfunction
Background: Atrial fibrillation (AF) is a common clinical arrhythmia associated with mitochondrial dysfunction, oxidative stress, and atrial fibrosis. Mitochondrial-derived peptides (MDPs), including humanin (HN) and MOTS-c, exhibit cytoprotective properties, but their role in AF remains largely unknown.
Study · 2026
MOTS-c is associated with oxidative stress and arterial stiffness in peritoneal dialysis patients: a pilot study
Purpose Oxidative stress (OS) and endothelial dysfunction are major drivers of cardiovascular disease (CVD) in peritoneal dialysis (PD).
Study · 2026
Elevated Serum Nardilysin Is Inversely Associated with Cardiovascular Disease in Kidney Transplant Recipients
Background Kidney transplant recipients (KTRs) suffer from enhanced cardiovascular (CV) and metabolic burden due to interplay between pro-inflammatory and metabolic risk factors.