Reviews MOTS-c

every claim, traced to its source

MOTS-c peptide: study references

The peer-reviewed studies and authoritative regulatory pages cited across this review, listed in full.

Back to the researchRead the bone-metabolism lens

How this list is used

Every quantitative claim on this site maps to a numbered entry below. Peer-reviewed studies are linked to PubMed with their DOI; the regulatory facts on the MOTS-c legal status page cite FDA pages directly. Where a finding is a review rather than a primary experiment, the entry says so.

Cited sources

The complete reference list is rendered from the structured citation data for this review. Entries 1 through 16 are peer-reviewed studies and reviews on MOTS-c; entries 17 through 19 are the FDA regulatory sources behind the legal-status page.

  1. Lee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, Cohen P. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015;21(3):443-454. ↗
  2. Reynolds JC, Lai RW, Woodhead JST, Joly JH, Mitchell CJ, Cameron-Smith D, Lu R, Cohen P, Graham NA, Benayoun BA, Merry TL, Lee C. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nat Commun. 2021;12(1):470. ↗
  3. Kim KH, Son JM, Benayoun BA, Lee C. The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress. Cell Metab. 2018;28(3):516-524.e7. ↗
  4. Wan W, Zhang L, Lin Y, Rao X, Wang X, Hua F, Ying J. Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging. J Transl Med. 2023;21(1):36. ↗
  5. Ming W, Lu G, Sha X, et al. Mitochondria related peptide MOTS-c suppresses ovariectomy-induced bone loss via AMPK activation. Biochem Biophys Res Commun. 2016;476(4):412-419. ↗
  6. Yi X, Hu G, Yang Y, Li J, Jin J, Chang B. Role of MOTS-c in the regulation of bone metabolism. Front Physiol. 2023;14:1149120. ↗
  7. Lu H, Wei M, Zhai Y, Li Q, Ye Z, Wang L, Luo W, Chen J, Lu Z. MOTS-c peptide regulates adipose homeostasis to prevent ovariectomy-induced metabolic dysfunction. J Mol Med (Berl). 2019;97(4):473-485. ↗
  8. Che N, Qiu W, Wang JK, Sun XX, Xu LX, Liu R, Gu L. MOTS-c improves osteoporosis by promoting the synthesis of type I collagen in osteoblasts via TGF-beta/SMAD signaling pathway. Eur Rev Med Pharmacol Sci. 2019;23(8):3194-3201. ↗
  9. Domin R, Pytka M, Ruchala M. MOTS-c Serum Concentration Positively Correlates with Lower-Body Muscle Strength and Is Not Related to Maximal Oxygen Uptake - A Preliminary Study. Int J Mol Sci. 2023;24(19):14951. ↗
  10. Mohtashami Z, Singh MK, Salimiaghdam N, Ozgul M, Kenney MC. MOTS-c, the Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases. Int J Mol Sci. 2022;23(19):11991. ↗
  11. Lee C. Nuclear transcriptional regulation by mitochondrial-encoded MOTS-c. Mol Cell Oncol. 2019;6(2):e1549464. ↗
  12. Editorial synthesis of MOTS-c evidence limitations and controversies (no completed human efficacy or safety trials; no validated human pharmacokinetics; research-chemical status with supplier-variable purity; WADA/USADA anti-doping prohibition; single-lab and small-sample reliance for some findings; the m.1382A>C pro-diabetogenic variant and ancestry-dependent responses), drawn from the cited reviews (Wan 2023, J Transl Med; Mohtashami 2022; Zheng 2023) and the compound compliance record. ↗
  13. Kumagai H, Kim SJ, Miller B, et al. MOTS-c modulates skeletal muscle function by directly binding and activating CK2. iScience. 2024;27(11):111212. ↗
  14. Bolignano D, Greco M, Presta P, Duni A, et al. The Mitochondrial-Derived Peptide MOTS-c May Refine Mortality and Cardiovascular Risk Prediction in Chronic Hemodialysis Patients: A Multicenter Cohort Study. Blood Purif. 2024. ↗
  15. Li K, Yang T, Chen F, et al. MOTS-c attenuates mitochondrial dysfunction, induces pyroptosis and cartilage degradation in osteoarthritis via an Nrf2-Dependent Mechanism. Free Radic Biol Med. 2025. ↗
  16. Zheng Y, Wei Z, Wang T. MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation. Front Endocrinol (Lausanne). 2023;14:1120533. ↗
  17. U.S. Food and Drug Administration. Bulk Drug Substances Used in Compounding Under Section 503A of the FD&C Act. FDA; verified 2026-05-29. ↗
  18. U.S. Food and Drug Administration. Human Drug Compounding — Section 503A patient-specific compounding and Section 503B outsourcing facilities (the lawful prescriber-evaluation, prescription, and dispensing pathway). FDA; verified 2026-05-29. ↗
  19. U.S. Food and Drug Administration. July 23-24, 2026: Meeting of the Pharmacy Compounding Advisory Committee — agenda lists BPC-157, KPV, TB-500, and MOTS-c as bulk drug substances being considered for inclusion on the 503A Bulks List. FDA; verified 2026-05-29 (a scheduled discussion, not a decision). ↗