Comparison
Degarelix vs. MOTS-c
Two peptides side-by-side — identity, evidence base, legal status and known adverse events.
Identity
Category
Research other
Research other
CAS no.
214766-78-6
1627580-64-6
Molecular weight
1632.3 g/mol
2174.61 g/mol
Half-life
1320 h
no data
Sequence
Ac-D-2Nal-D-4Cpa-D-3Pal-Ser-4Aph(Hor)-D-4Aph(Cbm)-Leu-Ilys-Pro-D-Ala-NH2Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-ArgMechanism of action
Degarelix
Degarelix is a competitive GnRH receptor antagonist. It binds reversibly and immediately to the pituitary GnRH receptors and blocks their activation. This rapidly suppresses the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which in turn lowers testosterone production in the testes. Unlike GnRH agonists (e.g., leuprorelin), which first cause a transient stimulation with a testosterone surge (flare), this direct antagonism lacks the initial stimulation phase, so testosterone declines without a preceding rise. This mechanism underlies the literature-described use in hormone-dependent prostate cancer.
MOTS-c
MOTS-c arises from a short open reading frame located in the 12S rRNA region of the mitochondrial genome — unlike most peptides it is therefore not encoded by nuclear DNA. Mechanistically, preclinical work describes MOTS-c as modulating the folate cycle and the de novo purine biosynthesis tethered to it, thereby affecting the AMP/ATP ratio and, downstream, AMP-activated protein kinase (AMPK). Under metabolic stress, an AMPK-dependent translocation of the peptide into the cell nucleus and involvement in the regulation of stress-responsive genes (including via antioxidant-response-element-regulated transcription factors) have also been reported. These models derive predominantly from cell culture and rodents; the extent to which they reflect human physiology after administration of exogenous synthetic MOTS-c is not established by human studies.
Evidence base
Highest evidence
Human RCT
Human trial
Studies
4
4
of which in humans
4
1
Effects recorded
4
4
Open conflicts
1
1
Documented adverse events
2
1
Legal status
Full entries
Frequently asked questions
- What is the difference between Degarelix and MOTS-c?
- Degarelix is classified as "Research other", while MOTS-c is classified as "Research other". Degarelix: Degarelix (trade name Firmagon) is a synthetic decapeptide and a gonadotropin-releasing hormone (GnRH) receptor antagonist. Unlike GnRH agonists, it blocks the receptor directly and does not trigger an initial testosterone surge (flare). It is an approved prescription medicine for the treatment of advanced, hormone-dependent prostate cancer. This page neutrally summarizes the evidence base and legal status and is not a usage or dosing recommendation. MOTS-c: MOTS-c is a 16-amino-acid mitochondrial-encoded peptide (mitochondrial-derived peptide, MDP) whose open reading frame lies within the 12S rRNA region of mitochondrial DNA. In basic research (including the laboratories of Changhan Lee and Pinchas Cohen) it is described as a regulator of metabolic homeostasis and an activator of the AMPK pathway, and is sometimes discussed as an 'exercise mimetic'. The evidence comes almost entirely from cell and animal models; controlled human trials of MOTS-c as a therapeutic are lacking. It is not approved as a medicine anywhere and is traded on the grey market as a research chemical. This page contrasts both neutrally and source-based — with no usage or dosing recommendation.
- Which peptide is better supported by science, Degarelix or MOTS-c?
- The highest available evidence level is "Human RCT" for Degarelix and "Human trial" for MOTS-c. A higher evidence level means more robust data, but says nothing about suitability for an individual. The full body of evidence is on each peptide's own page.
- What is the legal status of Degarelix and MOTS-c in Germany and the United States?
- Germany: Degarelix — Prescription, MOTS-c — Unapproved. United States: Degarelix — Prescription, MOTS-c — Unapproved. These are factual summaries with source and review date on the individual pages.