# MOTS-c peptide References: The Cited Study List

> MOTS-c peptide references: the full cited source list behind this review, with journals, years, DOIs, PubMed links, and the FDA regulatory pages.

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

## 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](/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.

## References

[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. https://pubmed.ncbi.nlm.nih.gov/25738459/
[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. https://pubmed.ncbi.nlm.nih.gov/33473109/
[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. https://pubmed.ncbi.nlm.nih.gov/29983246/
[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. https://pubmed.ncbi.nlm.nih.gov/36670507/
[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. https://pubmed.ncbi.nlm.nih.gov/27237975/
[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. https://pubmed.ncbi.nlm.nih.gov/37200834/
[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. https://pubmed.ncbi.nlm.nih.gov/30725119/
[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. https://pubmed.ncbi.nlm.nih.gov/31081069/
[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. https://pubmed.ncbi.nlm.nih.gov/37834399/
[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. https://pubmed.ncbi.nlm.nih.gov/36233287/
[11] Lee C. Nuclear transcriptional regulation by mitochondrial-encoded MOTS-c. Mol Cell Oncol. 2019;6(2):e1549464. https://pubmed.ncbi.nlm.nih.gov/31131297/
[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. https://pubmed.ncbi.nlm.nih.gov/36670507/
[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. https://pubmed.ncbi.nlm.nih.gov/39559755/
[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. https://pubmed.ncbi.nlm.nih.gov/39111290/
[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. https://pubmed.ncbi.nlm.nih.gov/41043625/
[16] Zheng Y, Wei Z, Wang T. MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation. Front Endocrinol (Lausanne). 2023;14:1120533. https://pubmed.ncbi.nlm.nih.gov/36936170/
[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. https://www.fda.gov/drugs/human-drug-compounding/bulk-drug-substances-used-compounding-under-section-503a-fdc-act
[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. https://www.fda.gov/drugs/guidance-compliance-regulatory-information/human-drug-compounding
[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). https://www.fda.gov/advisory-committees/advisory-committee-calendar/july-23-24-2026-meeting-pharmacy-compounding-advisory-committee-07232026

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A vivid market-stall review of the MOTS-c literature — each metabolism, exercise and bone study set out on its own painted card and cited to source, the empty human-trial line left in plain view, and the FDA 503A standing read off the PCAC agenda; no clinic behind the stall and nothing here dispensed or sold.