MOTS-C [Nasal Spray]

Description

What is MOTS-c Nasal Spray?

MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA-c) is a 16-amino acid peptide with the sequence MRWQEMGYIFYPRKLR. It is encoded by a short open reading frame (sORF) within the mitochondrial 12S ribosomal RNA gene (MT-RNR1) and represents one of a class of peptides now characterized as mitochondrial-derived peptides (MDPs). MOTS-c was first reported in 2015 by Changhan Lee, Pinchas Cohen, and colleagues at the Leonard Davis School of Gerontology, University of Southern California, as the first mitochondria-encoded peptide demonstrated to translocate to the cell nucleus and directly regulate nuclear gene expression in response to metabolic stress. Its amino acid sequence is highly conserved across 14 species, including humans and mice, particularly within the first 11 residues. Unlike nuclear DNA-encoded peptides, MOTS-c is translated from a polyadenylated mRNA transcript exported from the mitochondria and translated in the cytoplasm using the universal genetic code. MOTS-c has not been approved as a registered pharmaceutical in any country and has not been approved by the Food and Drug Administration for any indication.

MOTS-c has been investigated in C57BL/6J and C57BL/6N mouse model systems across a range of ages, in high-fat diet obesity preparations, and in spared nerve injury (SNI) neuropathic pain mouse preparations for its effects on skeletal muscle glucose uptake, AMPK activation, insulin sensitivity, physical capacity and exercise performance, age-dependent physical decline, and spinal cord neuroinflammation and neuropathic pain signaling. In human subjects, exercise has been shown to induce endogenous MOTS-c expression in skeletal muscle and in circulation, characterizing it as an exercise-induced mitokine. MOTS-c’s primary cellular target is skeletal muscle, where it modulates folate cycle metabolism and downstream AMPK activation.

The nasal spray formulation is investigated as a delivery route in preclinical research contexts, based on evidence of olfactory bulb-mediated CNS transport for peptide compounds administered intranasally in rodent models. Intranasal delivery has been studied for its potential to bypass hepatic first-pass metabolism and enhance CNS bioavailability relative to systemic routes in preclinical pharmacokinetic models. The nasal mucosa’s proximity to the central nervous system via the olfactory nerve makes it a research-relevant delivery route for CNS-active research compounds.

DISCLAIMER: MOTS-c Nasal Spray, as supplied by RCDbio, is not a dietary supplement and has not been approved by the Food and Drug Administration for human use, veterinary use, consumption, or any therapeutic application. This product is not intended for human consumption or therapeutic self-administration. It is supplied exclusively for in vitro and preclinical laboratory research purposes. All RCDbio research compounds are for laboratory and research purposes only.

Chemical Properties of MOTS-c

Property	Details
Product Type	Synthetic Mitochondrial-Derived Peptide (MDP) / Exercise Mimetic / AMPK Activator / Mitokine
Product Name	MOTS-c Nasal Spray
Application	Scientific / Research Use Only
CAS Number	1627580-64-6
Molar Mass	2174.62 g/mol
Chemical Formula	C101H152N28O22S2
IUPAC Name	(4S)-4-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-4-methylsulfanylbutanoyl]amino]-5-carbamimidamidopentanoyl]amino]-3-(1H-indol-3-yl)propanoyl]amino]-5-oxopentanoyl]amino]-5-[[(2S)-1-[[2-[[(2S)-1-[[(2S,3S)-1-[[(2S)-1-[[(2S)-1-[(2S)-2-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(1S)-4-carbamimidamido-1-carboxybutyl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]carbamoyl]pyrrolidin-1-yl]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-5-oxopentanoic acid (PubChem CID 146675088)
Synonyms	MOTS-c; Mitochondrial ORF of the 12S rRNA-c; MT-RNR1-encoded peptide; Mitochondrial Open Reading Frame Peptide Type-C; Exercise Mimetic Peptide; MRWQEMGYIFYPRKLR
Physical Form	Lyophilized white to off-white powder (compound); supplied as aqueous nasal spray solution
Solubility	Soluble in sterile water and 0.9% saline at ≥1 mg/mL
Storage (Lyophilized)	-20°C, desiccated, protected from light
Storage (Reconstituted / Nasal Spray)	2-8°C; use within 28 days of first actuation; DO NOT FREEZE; protect from light; keep upright
PubChem CID	146675088
Purity	≥98% (HPLC verified, independent third-party laboratory analysis; COA available per batch)
WADA Status	PROHIBITED – 2026 WADA Prohibited List, Category S4.4.1 (Metabolic Modulators – Activators of the AMP-activated protein kinase). MOTS-c is explicitly named by its full designation: “mitochondrial open reading frame of the 12S rRNA-c (MOTS-c).”  This prohibition applies both in and out of competition for all WADA Code signatories. No Therapeutic Use Exemption is available. RCDbio products are for laboratory research purposes only and are not supplied for use in competitive sport contexts.

How Does MOTS-c Work?

MOTS-c acts as a mitochondria-to-nucleus signaling peptide that modulates cellular metabolism through AMPK activation, folate cycle pathway inhibition, and direct nuclear gene regulation. Under resting conditions, MOTS-c is localized to mitochondria. Under metabolic stress conditions, it translocates to the nucleus and regulates antioxidant response element (ARE)-containing genes. Its primary target tissue is skeletal muscle, where it promotes glucose uptake via GLUT4 translocation and modulates folate-methionine cycle metabolism. No single confirmed receptor mediates MOTS-c activity; its effects are intracellular and depend on AMPK phosphorylation state and nuclear transcriptional regulation. The following mechanistic observations are from preclinical and in vitro data only.

Folate Cycle Inhibition and AMPK Activation

MOTS-c exerts its primary metabolic effects by inhibiting the folate cycle and its tethered de novo purine biosynthesis pathway in skeletal muscle cells. This inhibition leads to accumulation of AICAR (5-aminoimidazole-4-carboxamide ribonucleotide), an endogenous AMP analog that activates AMP-activated protein kinase (AMPK). AMPK activation drives glucose uptake via GLUT4 translocation to the plasma membrane, fatty acid oxidation, and suppression of anabolic pathways. This mechanism mirrors the cellular response to exercise and positions MOTS-c as an exercise mimetic in preclinical preparations [Lee et al., 2015; PMID 25738459].

Metabolic Homeostasis, Insulin Sensitivity, and Obesity Prevention

MOTS-c treatment in C57BL/6J mice prevented age-dependent and high-fat diet-induced insulin resistance, as well as diet-induced obesity. These effects were attributed to MOTS-c-mediated AMPK activation in skeletal muscle and downstream improvements in cellular glucose handling. MOTS-c treatment reduced obesity in high-fat diet preparations without adverse effects on lean mass in these mouse model preparations [Lee et al., 2015; PMID 25738459].

Exercise-Induced Mitokine and Age-Dependent Physical Decline

MOTS-c functions as an exercise-induced mitokine with age-dependent expression. In C57BL/6 mouse preparations across young (2 months), middle-aged (12 months), and old (22 months) cohorts, MOTS-c treatment significantly enhanced physical performance on treadmill running tests. Late-life initiated intermittent MOTS-c treatment (3x/week, starting at 23.5 months) increased physical capacity and healthspan markers in old mice. In human subjects, exercise induced endogenous MOTS-c expression in skeletal muscle and in circulation, with approximately 12-fold upregulation in skeletal muscle following exercise. MOTS-c regulated nuclear genes related to metabolism and proteostasis and modulated myoblast adaptation to metabolic stress [Reynolds et al., 2021; PMID 33473109].

AMPK-Dependent Neuropathic Pain Modulation and CNS Activity

In the spared nerve injury (SNI) mouse model of neuropathic pain, intrathecal MOTS-c administration produced dose-dependent antinociceptive effects. These effects were blocked by dorsomorphin (an AMPK inhibitor) but not by naloxone (an opioid receptor antagonist), confirming AMPK dependence and opioid-receptor independence. MOTS-c treatment enhanced AMPKalpha phosphorylation in the lumbar spinal cord, inhibited proinflammatory cytokine production, reduced microglia activation, and inhibited c-Fos expression and oxidative damage in spinal dorsal horn neurons [Jiang et al., 2023; PMID 37285113].

Intranasal Delivery & Pharmacokinetics

Olfactory Bulb-Mediated CNS Transport

When administered intranasally in preclinical rodent model systems, peptide compounds can access the central nervous system through the olfactory nerve (cranial nerve I) pathway. Compounds deposited on the olfactory mucosa are transported along olfactory axons through the cribriform plate to the olfactory bulb, from which access to deeper CNS structures has been characterized in rodent preparations. The olfactory and trigeminal nerve pathways for nose-to-brain peptide transport have been investigated in preclinical studies of peptide and protein delivery [Wong et al., 2024; PMID 38441832]. No compound-specific olfactory transport data for MOTS-c nasal spray have been published. MOTS-c’s documented CNS activity, including spinal cord AMPK modulation and nuclear translocation under metabolic stress, makes intranasal delivery pathway characterization a research-relevant consideration.

Hepatic First-Pass Metabolism Bypass

The intranasal route avoids portal circulation and hepatic first-pass metabolic processing. MOTS-c is a 16-amino acid linear peptide susceptible to proteolytic degradation in the GI environment. Intranasal delivery bypasses GI proteolytic exposure and hepatic first-pass extraction relevant to systemic peptide bioavailability. These observations do not constitute evidence of intranasal efficacy in human subjects.

Nasal Mucosal Absorption

MOTS-c has a molar mass of 2174.62 g/mol (approximately 2.17 kDa). This molecular weight falls within the lower 1-5 kDa bracket, indicating paracellular and endocytic uptake mechanisms are likely predominant absorption pathways at the nasal mucosa. At approximately 2.17 kDa, nasal mucosal absorption is expected to be less restricted by molecular weight than for larger research peptides in the RCDbio range. Specific nasal mucosal permeability coefficients for MOTS-c have not been published.

Compound-Specific Pharmacokinetics

No formal intranasal pharmacokinetic data for MOTS-c has been published in the peer-reviewed literature as of June 2026. Published preclinical research uses subcutaneous injection (15 mg/kg/day) or intrathecal administration. No human pharmacokinetic data has been published for any route of administration. The plasma half-life of MOTS-c following systemic injection has not been formally characterized in published preclinical studies. Researchers should account for the complete absence of published intranasal-specific pharmacokinetic parameters when designing laboratory protocols.

Key Research Findings

MOTS-c Promotes Metabolic Homeostasis and Reduces Obesity and Insulin Resistance via Folate Cycle/AMPK Pathway (C57BL/6J Mouse Preparations and In Vitro Cell Preparations): MOTS-c activated AMPK by inhibiting the folate cycle and de novo purine biosynthesis; prevented age-dependent and high-fat diet-induced insulin resistance; and reduced diet-induced obesity in C57BL/6J mouse model preparations; MOTS-c treatment promoted cellular glucose uptake and metabolic homeostasis [Lee et al., 2015; PMID 25738459]

MOTS-c is an Exercise-Induced Regulator of Age-Dependent Physical Decline and Muscle Homeostasis (C57BL/6 Mouse Preparations and Human Skeletal Muscle Exercise Response Data): MOTS-c significantly enhanced physical performance across young, middle-aged, and old mouse cohorts in treadmill preparations; late-life initiated intermittent treatment increased physical capacity in old mice; endogenous MOTS-c was upregulated approximately 12-fold in human skeletal muscle following exercise; MOTS-c regulated nuclear genes related to metabolism, proteostasis, and myoblast adaptation to metabolic stress [Reynolds et al., 2021; PMID 33473109]

MOTS-c Ameliorates Neuropathic Pain via AMPK-Dependent Spinal Cord Mechanism (Spared Nerve Injury Mouse Model): Intrathecal MOTS-c produced dose-dependent antinociceptive effects in SNI mice, blocked by AMPK inhibitor dorsomorphin but not by opioid antagonist naloxone; MOTS-c enhanced AMPKalpha phosphorylation in the lumbar spinal cord, inhibited proinflammatory cytokines, reduced microglia activation, and inhibited neuronal c-Fos expression and oxidative damage in the spinal dorsal horn [Jiang et al., 2023; PMID 37285113]

All findings listed above are from preclinical in vivo mouse model preparations and human exercise-response observations. Rows 1 and 2 used subcutaneous injection in mouse preparations. The human data in Row 2 describes endogenous MOTS-c upregulation by exercise, not exogenous administration. Row 3 used intrathecal injection in a mouse neuropathic pain model. These observations do not constitute evidence of efficacy or safety for the MOTS-c nasal spray formulation in any organism. No human clinical trial data for exogenous MOTS-c administration have been published as of June 2026.

What are the Potential Research Applications?

In controlled laboratory environments, MOTS-c nasal spray has been investigated for the following research applications. These are observed in preclinical and in vitro contexts only and do not constitute claims of efficacy or safety in any organism.

AMPK Signaling and Metabolic Pathway Research

MOTS-c is a physiologically relevant AMPK activator encoded in the mitochondrial genome. Research applications include AMPK phosphorylation assay systems in myoblast and skeletal muscle cell preparations, comparative folate cycle pathway studies in metabolic stress models, GLUT4 translocation and glucose uptake characterization in insulin-resistant cell preparations, and comparative pharmacology with other AMPK activators such as AICAR and metformin.

Exercise Mimetic and Physical Performance Research

MOTS-c’s characterization as an exercise-induced mitokine supports its use as a research tool in aging and physical performance model systems. Research applications include treadmill performance and physical capacity characterization in aged mouse preparations, muscle proteostasis and metabolic adaptability studies, comparative transcriptomic analyses of MOTS-c-treated versus exercised skeletal muscle preparations, and investigation of mitochondria-to-nucleus signaling in muscle homeostasis.

Aging and Metabolic Homeostasis Research

MOTS-c expression is age-dependent and detected across multiple tissues. Research applications include age-dependent insulin resistance and obesity model studies in high-fat diet mouse preparations, mitochondrial-nuclear communication pathway characterization, investigation of endogenous MOTS-c expression trajectories in aging tissues, and comparative studies with other mitochondrial-derived peptides, including humanin and SHLP.

CNS and Neuropathic Pain Research

MOTS-c’s AMPK-dependent CNS activity and nuclear translocation under metabolic stress support its investigation in CNS model systems. Research applications include neuropathic pain pathway studies via AMPK activation in spinal cord preparations, neuroinflammation and microglia activation assays, spinal dorsal horn oxidative stress characterization, and investigation of MOTS-c’s nuclear gene regulation in CNS cell preparations.

What are the Potential Side Effects?

Researchers in preclinical and in vitro settings have noted the following observations. Long-term safety and toxicity profiles remain incompletely characterized for the research-grade nasal spray formulation.

• Favorable preclinical safety profile in published mouse studies (preclinical): Published MOTS-c studies in mouse preparations at doses up to 15 mg/kg/day over multi-week treatment periods have not reported significant adverse effects; this observation does not constitute a formal toxicology assessment for the nasal spray formulation or for human use
• Hypoglycemia risk (class context): MOTS-c promotes AMPK activation and cellular glucose uptake in skeletal muscle; inadvertent intranasal self-exposure carries a theoretical risk of hypoglycemia, particularly in fasted states or in combination with other glucose-lowering research compounds
• WADA-przhibited status – systemic exercise-mimetic activity: MOTS-c is prohibited under WADA S4.4 due to its exercise-mimetic AMPK-activating properties; inadvertent intranasal self-exposure carries a risk of systemic AMPK activation and metabolic effects consistent with the rationale for its WADA prohibition
• Absence of intranasal-specific safety data: No safety or tolerability data specific to the intranasal route of administration for MOTS-c has been published in the peer-reviewed literature as of June 2026
• No completed human clinical trials for exogenous MOTS-c: No human Phase 1 safety or efficacy trials for synthetic MOTS-c have been completed or published as of June 2026; CB4211, a modified MOTS-c-derived analog, is structurally distinct, and its Phase 1 data should not be used as safety evidence for unmodified MOTS-c.

No human safety or tolerability data have been established for MOTS-c nasal spray. These observations are derived from experimental systems and should not be extrapolated to human or animal outcomes.

Risk & Handling

Handling Precautions

Standard laboratory PPE is required: nitrile gloves, a laboratory coat, and eye protection. The following nasal spray-specific precautions apply:

1. Do not direct the nasal spray actuator toward the face, eyes, or mucous membranes during handling, testing, or transfer. MOTS-c is WADA-prohibited due to AMPK-mediated exercise-mimetic activity; inadvertent intranasal self-exposure may produce systemic metabolic effects.
2. Handle the nasal spray solution in a clean laboratory environment. For aliquoting or analytical sampling, use a laminar flow cabinet.
3. The nasal spray solution is an aqueous formulation susceptible to microbial contamination if compromised. Handle under aseptic conditions. Discard if the solution appears cloudy, discolored, or shows particulate matter.
4. Avoid aerosol generation during any manipulation of the nasal spray solution.

Exposure Risks

Risk Tier: LOW-MODERATE

MOTS-c is a physiologically active AMPK activator with systemic metabolic effects documented across multiple organ systems in preclinical preparations. Inadvertent intranasal self-exposure carries a theoretical risk of AMPK-mediated hypoglycemia and systemic metabolic modulation. Published preclinical mouse studies have not reported significant adverse effects at research doses. No human safety or tolerability data have been established for MOTS-c nasal spray. Researchers should handle this compound with precautions appropriate to a metabolically active peptide hormone with WADA-prohibited exercise-mimetic activity.

Storage

In-use nasal spray: Store at 2-8°C. Use within 28 days of first actuation. Protect from light. Keep upright.

DO NOT FREEZE the ready-to-use nasal spray formulation. Freezing alters pH, buffer stability, excipient integrity, and spray actuation properties.

Lyophilized bulk stock (if applicable): Store at -20°C in sealed, desiccated, light-protected containers. Avoid repeated freeze-thaw cycles.

Discard any solution that appears cloudy, discolored, or shows visible particulate matter.

FAQs

Q: How does intranasal administration facilitate the delivery of MOTS-c in preclinical research models?

A: Intranasal application bypasses hepatic first-pass metabolism and the GI proteolytic environment, relevant given MOTS-c’s susceptibility to proteolytic degradation as a linear 16-amino acid peptide. The olfactory and trigeminal nerve pathways for peptide transport have been characterized for structurally related peptide compounds in rodent models [Wong et al., 2024; PMID 38441832]. MOTS-c’s documented CNS activity, including spinal cord AMPK modulation, supports intranasal delivery as a research-relevant pathway. No compound-specific intranasal olfactory transport data exist for MOTS-c.

Q: What is the recommended storage and in-use shelf life for MOTS-c nasal spray?

A: Sealed product should be stored at 2-8°C, protected from light. Once first actuated, in-use shelf life is 28 days at 2-8°C. DO NOT FREEZE the ready-to-use solution. Lyophilized bulk stock should be stored at -20°C in sealed, desiccated, light-protected conditions. Discard if the solution shows cloudiness, discoloration, or particulate matter.

Q: Is the MOTS-c nasal spray formulation suitable for cell culture or in vitro assay systems?

A: The formulation is prepared in isotonic saline (0.9% NaCl, pH 6.0-7.0) without preservatives. Dilution into culture medium before application is recommended to normalize pH. MOTS-c promotes AMPK activation in myoblast and skeletal muscle cell preparations; researchers should account for this metabolic activity in assay design. Researchers are responsible for confirming compatibility with their assay system.

Q: What distinguishes MOTS-c from other mitochondrial-derived peptides such as humanin?

A: MOTS-c is encoded by the 12S rRNA region of mitochondrial DNA and acts via folate cycle inhibition and AMPK activation, with skeletal muscle as its primary target. Humanin is encoded by the 16S rRNA region and acts via STAT3 and IGF-1 receptor pathways with anti-apoptotic and neuroprotective effects. MOTS-c is the only MDP demonstrated to translocate to the cell nucleus under metabolic stress and directly regulate nuclear gene expression.

Q: What is the WADA status of MOTS-c?

A: MOTS-c is prohibited under the 2026 WADA Prohibited List, Category S4.4.1 (Metabolic Modulators — Activators of the AMP-activated protein kinase), explicitly named since January 1, 2024. This prohibition applies both in and out of competition for all WADA Code signatories. No Therapeutic Use Exemption is available. RCDbio products are supplied for laboratory research purposes only and are not supplied for use in competitive sport contexts.

Q: What is the FDA regulatory status of MOTS-c?

A: MOTS-c is not FDA-approved for any indication. As of June 2026, its 503A Category 2 nomination was withdrawn in April 2026, and it is scheduled for PCAC evaluation in July 2026. CB4211, a modified MOTS-c-derived analog by CohBar Inc., is structurally distinct from unmodified synthetic MOTS-c; CB4211 Phase 1 data should not be extrapolated to unmodified MOTS-c. The research-grade nasal spray supplied by RCDbio is for laboratory research use only.

Q: What is the significance of MOTS-c being mitochondria-encoded, and how does that affect its research relevance?

A: MOTS-c is encoded by the mitochondrial 12S rRNA gene (MT-RNR1), making it one of a small class of signaling peptides derived from the mitochondrial genome. It is the only MDP demonstrated to translocate to the cell nucleus and regulate nuclear gene expression under metabolic stress, establishing bidirectional mitochondria-nuclear communication as an active regulatory mechanism. Human skeletal muscle MOTS-c levels rise approximately 12-fold following exercise, characterizing it as an exercise-induced mitokine with implications for aging, metabolism, and physical performance research.

Related Research Compounds

Researchers investigating MOTS-c nasal spray may also be interested in the following compounds currently available for laboratory research at RCDbio:

Liraglutide (GLP-1) Nasal Spray – A GLP-1 receptor agonist investigated in preclinical preparations for insulin resistance improvement, beta cell mass preservation, and metabolic pathway modulation via GLP-1R/cAMP signaling in complementary metabolic research contexts.

HGH Fragment 176-191 Nasal Spray – A synthetic C-terminal growth hormone peptide investigated in preclinical preparations for hGH receptor-independent lipolysis and lipid metabolism signaling in adipocyte model systems.

BPC-157 Nasal Spray– A stable gastric pentadecapeptide investigated in preclinical rodent preparations for cytoprotection, NO-system modulation, and tissue healing via intranasal delivery.

All products listed are for laboratory and research purposes only.

References

1. Lee, C., Zeng, J., Drew, B.G., Sallam, T., Martin-Montalvo, A., Wan, J., Kim, S.J., Mehta, H., Hevener, A.L., de Cabo, R., & Cohen, P. (2015). The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism, 21(3), 443-454.

   https://pubmed.ncbi.nlm.nih.gov/25738459/

2. Reynolds, J.C., Lai, R.W., Woodhead, J.S.T., Joly, J.H., Mitchell, C.J., Cameron-Smith, D., Lu, R., Cohen, P., Graham, N.A., Benayoun, B.A., Merry, T.L., & Lee, C. (2021). MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nature Communications, 12(1), 470.

   https://pubmed.ncbi.nlm.nih.gov/33473109/

3. Jiang, J., Xu, L., Yang, L., Liu, S., & Wang, Z. (2023). Mitochondrial-derived peptide MOTS-c ameliorates spared nerve injury-induced neuropathic pain in mice by inhibiting microglia activation and neuronal oxidative damage in the spinal cord via the AMPK pathway. ACS Chemical Neuroscience, 14(12), 2362-2374.

   https://pubmed.ncbi.nlm.nih.gov/37285113/

4. Wong, C.Y.J., Baldelli, A., Hoyos, C.M., et al. (2024). Insulin delivery to the brain via the nasal route: unraveling the potential for Alzheimer’s Disease therapy. Drug Delivery and Translational Research, 14(7), 1776-1793.

   https://pubmed.ncbi.nlm.nih.gov/38441832/

Research Transparency Note: No peer-reviewed publications specific to intranasal delivery of MOTS-c are available as of June 2026. References 1 and 2 describe subcutaneous injection in mouse model preparations. Reference 3 describes intrathecal administration in a neuropathic pain mouse model; this is not equivalent to intranasal delivery but supports MOTS-c’s CNS research relevance. The exercise-response human data in Reference 2 describes endogenous MOTS-c upregulation by exercise, not exogenous administration. The olfactory transport pathway evidence in Reference 4 is class-level. CB4211 (a modified MOTS-c-derived analog) is structurally distinct from unmodified MOTS-c; CB4211 Phase 1 data should not be applied to synthetic MOTS-c nasal spray.

Disclaimer

MOTS-c Nasal Spray is exclusively for laboratory research purposes. RCDbio products are not intended to diagnose, prevent, treat, or cure any disease or medical condition.

The Food and Drug Administration has not evaluated the statements on our website. This product is not approved for human or veterinary use. Researchers must comply with all applicable local, state, and federal laws and regulations governing the purchase and use of research compounds. By purchasing, you agree to our Terms and Conditions. RCDbio reserves the right to refuse sales to unauthorized individuals.

ATTENTION: All RCDbio products are strictly for LABORATORY AND RESEARCH PURPOSES ONLY. They are not intended for human consumption, veterinary use, or any other non-research application. For queries, complaints, or support, contact support@rcdbio.co