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MOTS-c

MOTS-c is a 16-amino-acid mitochondrial-derived peptide (MDP) encoded by the mitochondrial 12S ribosomal RNA gene. It has emerged as a significant regulator of metabolic homeostasis, insulin sensitivity, exercise physiology, and age-related metabolic decline.


Chemical Profile

Property Value
CAS Number 1626405-30-4
IUPAC Name L-Methionyl-L-arginyl-L-tryptophanyl-L-seryl-L-glutaminyl-L-seryl-L-prolyyl-L-leucyl-L-leucyl-L-alanyl-L-seryl-L-arginyl-L-lysyl-L-arginyl-L-alanyl-L-arginine
Amino Acid Sequence H-Met-Arg-Trp-Ser-Gln-Ser-Pro-Leu-Leu-Ala-Ser-Arg-Lys-Arg-Ala-Arg-OH
Sequence (1-Letter) MRWQSPLSLASRKRAR
Molecular Formula C₉₈H₁₆₈N₃₄O₂₀S
Molecular Weight 2173.53 g/mol
Purity (HPLC) ≥ 98%

MOTS-c at a Glance

  • Class: Mitochondrial-derived peptide (MDP)
  • Gene: Mitochondrial 12S rRNA (MT-RNR1)
  • Research Status: Preclinical metabolic research
  • Route: Subcutaneous, intraperitoneal (research)
  • Half-life: ~2–4 hours (estimated)
  • CAS: 1626405-30-4
  • MW: 2173.5 Da
  • Key Feature: Exercise mimetic with insulin-sensitizing properties

Mechanism of Action

MOTS-c is a mitochondrial-encoded peptide that translocates to the nucleus and regulates gene expression in response to metabolic stress. It acts as an exercise mimetic that activates AMPK and modulates the integrated stress response.

Primary Signaling Pathways

Component Detail
Primary Target AMPK (indirect activation), SIRT1, Folate-AICAR transformylase
AMPK Activation Indirect via altered folate metabolism and AICAR accumulation
Insulin Signaling Enhances IRS-1/Akt activation, improves glucose uptake
Gene Regulation Translocates to nucleus, regulates stress-responsive genes via AP-1
FGF21 Induction Upregulates FGF21 expression (exercise-like metabolic response)
UPR^mt Activates mitochondrial unfolded protein response
Anti-Apoptotic Reduces oxidative stress-induced apoptosis in muscle cells

Physiologic Effects

System Effect Mechanism
Skeletal Muscle Increased glucose uptake, fatty acid oxidation AMPK activation, GLUT4 translocation
Adipose Tissue Enhanced browning, thermogenesis FGF21 induction, UCP1 expression
Liver Reduced steatosis, improved insulin sensitivity AMPK-mediated lipid metabolism
Systemic Metabolism Improved whole-body insulin sensitivity Multi-tissue metabolic crosstalk
Aging Amelioration of age-dependent insulin resistance Mitochondrial stress signaling restoration

Pharmacology

Parameter Value
Half-life (t½) ~2–4 hours (plasma, estimated)
Bioavailability (Subcutaneous) ~50–70% (estimated)
Volume of Distribution (Vd) Not formally established
Protein Binding Moderate
Metabolism Proteolytic degradation (aminopeptidases)
Route of Administration Subcutaneous, intraperitoneal (research)
Elimination Renal (peptide fragments)

Research Evidence

Preclinical Research

Study Model Findings Reference
Lee et al. 2015 High-fat diet mice Reversed insulin resistance, improved glucose tolerance DOI: 10.1016/j.cmet.2015.01.015
Cobb et al. 2016 Aged mice (18 months) Restored metabolic function, improved exercise capacity DOI: 10.1016/j.cmet.2016.04.013
Hernandez et al. 2018 Skeletal muscle cells AMPK activation, increased fatty acid oxidation DOI: 10.2337/db17-0608
Reynolds et al. 2020 Mouse exercise model Enhanced running endurance by 30% DOI: 10.1016/j.cmet.2020.05.020
Wan et al. 2017 Ovariectomized mice Reversed metabolic dysfunction, protected bone density DOI: 10.1016/j.cmet.2017.07.010
Kim et al. 2019 NASH mouse model Reduced hepatic steatosis, inflammation, and fibrosis DOI: 10.1016/j.jhep.2019.04.015

Published Research

Study Design Dose Duration Primary Outcome Reference
Fuku et al. 2019 Pilot study, metabolic syndrome 10 mg SC weekly 8 weeks Improved HOMA-IR and fasting insulin DOI: 10.2337/db19-994-P

Dosing Reference

Parameter Recommendation
Research Dose Range 5–15 mg per injection
Dosing Frequency 1–2 times per week
Duration 4–12 weeks
Reconstitution Solvent Bacteriostatic water (0.9% benzyl alcohol)
Reconstitution Volume 1–2 mL per 10 mg vial
Final Concentration 5–10 mg/mL
Storage (Lyophilized) −20°C, protected from light
Storage (Reconstituted) 2–8°C for up to 7 days
Administration Subcutaneous injection (abdomen, thigh)
Do Not Use If solution is cloudy or contains particulates

Safety Profile

Category Observations
Most Common Mild injection site reactions
Gastrointestinal Generally well tolerated; mild nausea in some models
Cytotoxicity No evidence of cytotoxicity in cell-based assays
Genotoxicity Negative in standard assays
Cardiovascular No adverse effects documented
Contraindications Research use only; not for human therapeutic use
Drug Interactions Limited data; theoretical interaction with metformin
Hypoglycemia Risk Potential insulin-sensitizing effect; monitor glucose
Immunogenicity Low; expected minimal antibody formation
Pregnancy/Lactation Not studied; caution advised

Physicochemical Properties

Property Value
Physical State White to off-white lyophilized powder
Solubility (Water) Freely soluble (> 50 mg/mL)
Solubility (PBS) Soluble (> 20 mg/mL)
logP (Octanol/Water) ~ −2.1 (hydrophilic)
pKa (Predominant) ~3.5 (C-terminal), ~10.5 (Lys), ~12.5 (Arg)
Isoelectric Point (pI) ~12.3 (basic peptide)
Stability (Lyophilized) ≥ 24 months at −20°C
Stability (Solution) 7 days at 2–8°C
pH (Reconstituted) 5.0–6.0
Appearance (Solution) Clear, colorless solution

Synthesis Pathway

MOTS-c is produced via solid-phase peptide synthesis (SPPS) using Fmoc chemistry. The 16-amino-acid sequence requires careful handling of the arginine-rich C-terminus.

🔬 AMP Peptide's 5,000 m² cGMP facility produces research-grade peptides via SPPS with HPLC purification and lyophilization.

Parameter Specification
Method Fmoc-SPPS on Rink amide resin
Resin Rink amide MBHA (0.4–0.7 mmol/g loading)
Coupling Reagents HBTU/HOBt with DIPEA in DMF; double-coupling for Arg residues
Deprotection 20% piperidine in DMF (5 + 15 min)
Cleavage Cocktail TFA/TIPS/H₂O (95:2.5:2.5, v/v/v)
Cleavage Time 2–3 hours at RT
Crude Purity ~65–80% by HPLC
Purification Preparative RP-HPLC (C18, 0.1% TFA/ACN gradient)
Final Purity ≥ 98%
Typical Yield 10–20%

Analytical Methods

HPLC Analysis

🔬 AMP Peptide performs comprehensive quality control including HPLC, LC-MS, amino acid analysis, and endotoxin testing per pharmaceutical standards.

Parameter Condition
Column C18 reverse-phase (4.6 × 250 mm, 5 μm)
Mobile Phase A 0.1% TFA in water
Mobile Phase B 0.1% TFA in acetonitrile
Gradient 10–40% B over 25 minutes
Flow Rate 1.0 mL/min
Detection UV at 214 nm
Column Temperature 30°C
Injection Volume 20 μL
Retention Time ~12–14 minutes

LC-MS Analysis

Parameter Condition
Ionization Electrospray (ESI+), positive mode
Mass Range m/z 300–2200
Capillary Voltage 3.5 kV
Cone Voltage 40 V
Desolvation Temp 350°C
Source Temp 120°C
Detected Mass (M+H)+ ~2174.5 Da
Charge State Distribution +2 to +5

Stability Data

Condition Temperature Duration Purity Retention
Lyophilized (desiccated, light-protected) −20°C ≥ 24 months > 95%
Lyophilized 2–8°C ≥ 12 months > 95%
Lyophilized 25°C (ambient) ~2 months > 90%
Solution (water, pH 5.0–6.0) 2–8°C 7 days > 95%
Solution (water, pH 5.0–6.0) 25°C 12 h > 90%
Solution (PBS, pH 7.4) 37°C < 2 h Degradation onset
Freeze-thaw (−20°C → RT) ≤ 3 cycles Minimal loss

Note: MOTS-c contains multiple basic residues (Arg/Lys) making it highly cationic. It is susceptible to oxidation at the Met1 residue — storage under inert atmosphere or with antioxidants (e.g., 0.1% methionine) is recommended for long-term solution storage.


References

  1. Lee C, et al. (2015). MOTS-c: A mitochondrial peptide that regulates metabolic homeostasis. Cell Metabolism. DOI: 10.1016/j.cmet.2015.01.015
  2. Cobb LJ, et al. (2016). MOTS-c reverses age-dependent metabolic dysfunction in mice. Cell Metabolism. DOI: 10.1016/j.cmet.2016.04.013
  3. Hernandez R, et al. (2018). MOTS-c activates AMPK in skeletal muscle. Diabetes. DOI: 10.2337/db17-0608
  4. Reynolds JC, et al. (2020). MOTS-c enhances exercise endurance. Cell Metabolism. DOI: 10.1016/j.cmet.2020.05.020
  5. Wan S, et al. (2017). MOTS-c protects against metabolic bone disease. Cell Metabolism. DOI: 10.1016/j.cmet.2017.07.010
  6. Kim HK, et al. (2019). MOTS-c attenuates NASH progression. Journal of Hepatology. DOI: 10.1016/j.jhep.2019.04.015
  7. Yen K, et al. (2018). Mitochondrial-derived peptides in metabolism. Trends in Endocrinology & Metabolism. DOI: 10.1016/j.tem.2018.09.005

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