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Peptide Research

Retatrutide: Triple Agonist for Metabolic Models

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Retatrutide is an experimental synthetic peptide, serving as a triple agonist for GLP-1, GIP, and glucagon receptors, derived from incretin analogs, and examined for its potential in obesity and metabolic dysfunction simulations.

Mechanism of Action: It mimics incretin hormones to promote glucose-dependent insulin secretion, suppress appetite, and boost lipid metabolism via synergistic receptor activation, with an extended half-life for sustained effects.

Interactions: It interfaces with insulin and glucagon-like pathways, enhancing insulin sensitivity and reducing hepatic inflammation; in experimental models, it synergizes with low-calorie diets to refine body composition.

Key Studies and Publications:

NAD+: Precursor for Cellular Metabolism

NAD+ (Nicotinamide Adenine Dinucleotide) is an essential coenzyme, not a traditional peptide but explored in peptide contexts for its effects on longevity, produced endogenously and declining with age.

Mechanism of Action: It serves as a substrate for sirtuins and PARP, regulating DNA repair, mitochondrial metabolism, and oxidative stress; an NAD+ boost activates anti-aging pathways such as autophagy.

Interactions: It interacts with NAD-dependent enzymes (e.g., SIRT1), modulating inflammation and neuroprotection; it shows synergy with precursors like NMN in aging models.

Key Studies and Publications:

GHK-Cu: Skin Regenerative Modulator

GHK-Cu (Glycyl-L-Histidyl-L-Lysine-Copper) is a naturally occurring copper-complexed tripeptide found in human plasma, acknowledged for its regenerative effects in experimental models of wound repair and cutaneous aging.

Mechanism of Action: It complexes with copper to stimulate metalloproteinases and angiogenesis, fostering the synthesis of collagen and elastin while mitigating inflammation through targeted gene expression modulation.

Interactions: Engages copper-dependent receptors to enhance tissue healing; exhibits synergistic effects with antioxidants in anti-inflammatory biological pathways.

Key Studies and Publications:

5-Amino-1MQ: NNMT Inhibitor for Metabolic Processes

5-Amino-1MQ is a compact molecule that acts as an inhibitor of nicotinamide N-methyltransferase (NNMT), examined for its potential role in experimental models of obesity and type 2 diabetes.

Mechanism of Action: It suppresses NNMT activity, limiting NAD+ methylation and enhancing glucose and lipid metabolism, which supports fat reduction and improved insulin sensitivity.

Interactions: It engages NAD+-related pathways, countering IL-1β-driven inflammation; shows promise in combination with dietary interventions for mitochondrial regeneration.

Key Studies and Publications:

MOTS-c: Mitochondrial-Derived Peptide for Longevity

MOTS-c is a 16-amino-acid peptide originating from mitochondrial DNA, encoded within the mtDNA genome, and investigated for its influence on metabolic control and age-related processes in preclinical models.

Mechanism of Action: It migrates to the nucleus to influence gene transcription through NRF2 activation, boosting glucose uptake, alleviating insulin resistance, and shielding mitochondria against oxidative damage.

Interactions: It binds to nuclear DNA sequences and ARE-binding transcription factors, supporting antioxidant responses; demonstrates metabolic impacts on lipid handling in diabetes-like experimental settings.

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TB-500 (Thymosin Beta-4): Tissue Regenerative Peptide

TB-500, also known as Thymosin Beta-4, is a naturally occurring 43-amino-acid peptide expressed in developing tissues, explored for its contributions to cellular migration and repair mechanisms in preclinical wound-healing models.

Mechanism of Action: It binds to actin to facilitate cell migration and proliferation, while supporting angiogenesis and stem cell differentiation to expedite wound closure.

Interactions: It modulates inflammatory responses and endothelial activity; displays cooperative effects with growth factors in muscle injury simulations.

Key Studies and Publications:

BPC-157: Gastric Protective Compound

BPC-157 is a synthetic pentadecapeptide derived from a protein in human gastric juice, recognized for its versatile effects in preclinical simulations of gastrointestinal injuries and musculoskeletal damage.

Mechanism of Action: It reinforces mucosal integrity and stimulates angiogenesis through enhanced growth hormone receptor expression, thereby curbing inflammation and hastening tissue recovery.

Interactions: It interfaces with serotonergic systems and VEGF signaling; provides safeguard effects on remote organs during ischemia-reperfusion scenarios.

Key Studies and Publications:

IGF-1 LR3: Muscle Growth Analog

IGF-1 LR3 represents a modified variant of Insulin-like Growth Factor-1, featuring an arginine extension for extended half-life, investigated for its hypertrophic potential in in vitro cellular models.

Mechanism of Action: It binds to IGF-1R receptors to activate the PI3K/Akt pathway, encouraging cellular proliferation and viability while countering atrophy.

Interactions: It synergizes with HGH; interacts with binding proteins to optimize bioavailability, offering protective outcomes in cardiovascular contexts.

Key Studies and Publications:

CJC-1295 + Ipamorelin

CJC-1295 (without DAC) is a short half-life GHRH analog used in research to stimulate physiological pulsatile GH release.
Ipamorelin is a selective GH secretagogue acting via the GHS-R1a (ghrelin) receptor, with minimal activation of cortisol and prolactin.

Mechanism:
Synergistic activation of two distinct upstream GH-axis pathways:
GHRH-R (CJC-1295) + GHS-R1a (Ipamorelin) → amplified GH release while preserving physiological endocrine feedback.

Interactions:
Hypothalamic–pituitary level action; rapid, controllable, pulsatile signaling without artificial pharmacokinetic extension (NO DAC).

Research context:
Modeling pulsatile GH secretion, studying GHRH–GHS synergy, and comparative analysis of upstream GH–IGF-1 axis mechanisms.

Studies & publications:
• Once-daily administration of CJC-1295 (PubMed, 2006)
• Ipamorelin, the first selective growth hormone secretagogue (PubMed, 1998)

SS - 31

SS-31 is a mitochondria-targeted tetrapeptide studied for its ability to stabilize mitochondrial function and reduce cellular oxidative stress.

Mechanism:
Selectively binds to cardiolipin in the inner mitochondrial membrane, improving electron transport chain efficiency and reducing reactive oxygen species (ROS) production.
Interactions:
Direct mitochondrial action; does not interact with nuclear or hormonal receptors.

Research context:
Studies on mitochondrial dysfunction, cellular energy metabolism, oxidative stress, and degenerative cellular models.

Studies & publications:

• Mitochondrial protein interaction landscape of SS-31 (PNAS, 2020)

• Elamipretide Improves Mitochondrial Function  (PubMed, 2026)

Semax

SEMAX is a neuroactive heptapeptide derived from ACTH (4–10), lacking systemic hormonal activity, studied as a neurosynaptic and neuroprotective modulator.

Mechanism:
Modulation of neurotrophic pathways (BDNF), regulation of glutamatergic and cholinergic transmission, and influence on neuronal gene expression.

Interactions:
Acts within the central nervous system; does not activate the HPA axis or corticosteroid receptors.

Research context:
Studies on synaptic plasticity, memory, neuronal stress, and neuroprotection models.

Studies & publications:

• Semax, an analogue of adrenocorticotropin (PubMed, 2006)

KPV: Anti-Inflammatory Tripeptide

KPV (Lys-Pro-Val) is a tripeptide derived from α-melanocyte-stimulating hormone (α-MSH), valued for its anti-inflammatory attributes in preclinical simulations of inflammatory bowel disease (IBD) and dermal inflammation.

Mechanism of Action: It inhibits NF-κB signaling and translocates into the nucleus to disrupt Imp-α3 interactions, thereby suppressing pro-inflammatory cytokine production.

Interactions: It engages pathways akin to MC3R receptors; collaborates with hyaluronic acid for optimized oral mucosal delivery.

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