Peptide guides

Every compound, characterized.

Ten research-grade peptides — each with a doctor-vetted summary of what published literature describes about mechanism, kinetics, and primary research. For qualified-researcher review only.

In this library

Retatrutide

aka LY3437943

Triple-agonist (GIP / GLP-1 / Glucagon). Next-generation triple-agonist studied for appetite regulation and metabolic-pathway research.

Retatrutide (LY3437943) is a next-generation triple-agonist research peptide engineered to bind three incretin and glucose-regulating receptors simultaneously — GIP, GLP-1, and glucagon. By recruiting all three pathways at once, Retatrutide is one of the most pharmacologically distinct compounds currently being investigated in metabolic-pathway research.

Current investigational literature highlights Retatrutide's potency in pre-clinical and early clinical weight-management and metabolic studies, where the addition of glucagon-receptor activity is hypothesized to compound the energy-expenditure effects already established for GIP/GLP-1 dual-agonism.

Mechanism summary

Retatrutide functions as a balanced agonist across three receptor populations:

  • GIP receptor — modulation of incretin signaling and insulin secretion
  • GLP-1 receptor — appetite regulation, satiety, gastric-emptying delay
  • Glucagon receptor — hypothesized to drive additional energy expenditure and hepatic lipid mobilization

The combined-receptor profile differentiates Retatrutide from earlier mono- (GLP-1) and dual-agonist (GIP/GLP-1) research peptides.

Primary literature

Tirzepatide

aka LY3298176

Dual-agonist (GLP-1 / GIP). Dual-receptor research peptide investigated for appetite, glycemic, and metabolic-pathway studies.

Tirzepatide (LY3298176) is a dual-agonist research peptide targeting both the GLP-1 and GIP receptors. The dual-receptor mechanism is studied for its compounding effects on appetite signaling, gastric emptying, and post-prandial glucose regulation — and has driven significant body-weight reductions in published clinical-research settings.

Tirzepatide remains one of the most heavily-studied incretin-class research compounds and forms a reference point for newer multi-agonist peptides such as Retatrutide.

Mechanism summary

Tirzepatide engages two complementary incretin receptors:

  • GLP-1 receptor — satiety, delayed gastric emptying, modulated insulin secretion
  • GIP receptor — incretin amplification, lipid-utilization pathways

The combined profile is studied for its capacity to amplify the metabolic effects of GLP-1 mono-agonism while reducing the GI-side-effect profile typically seen with high-dose GLP-1 alone.

Primary literature

Semaglutide

aka GLP-1 analogue

GLP-1 receptor agonist. Long-acting GLP-1 analogue widely studied for appetite, satiety, and metabolic research.

Semaglutide is a long-acting GLP-1 receptor agonist research peptide and one of the most extensively studied incretin compounds in modern metabolic literature. As a structural analogue of native GLP-1, Semaglutide is engineered for prolonged plasma half-life and enhanced receptor affinity.

Research applications span appetite regulation, satiety modeling, gastric-emptying kinetics, and post-prandial glucose-handling — making it a foundational reference compound in any GLP-1 research workflow.

Mechanism summary

Semaglutide selectively activates the GLP-1 receptor, producing:

  • Sustained satiety signaling via central GLP-1R populations
  • Slowed gastric emptying and modulated post-prandial glucose excursion
  • Insulin-secretion modulation in pancreatic β-cells

The Aib⁸ substitution and C18-diacid acylation extend half-life from minutes (native GLP-1) to roughly a week, making once-weekly research dosing feasible.

Primary literature

BPC-157

aka Bepecin · PL 14736

Body Protective Compound · pentadecapeptide. Gastric pentadecapeptide investigated for soft-tissue, gastric, and angiogenesis research.

BPC-157 (Body Protective Compound 157) is a synthetic pentadecapeptide derived from a sequence identified in human gastric juice. It is one of the most widely cited research peptides in the soft-tissue and gastric-repair literature.

Preclinical work has explored BPC-157 across models of tendon, ligament, and gastrointestinal injury, with mechanisms broadly tied to angiogenesis, nitric-oxide signaling, and growth-factor expression.

Mechanism summary

BPC-157's reported activity in pre-clinical literature includes:

  • Modulation of angiogenesis and capillary network formation
  • Up-regulation of the nitric-oxide (NO) pathway and VEGF expression
  • Enhanced fibroblast migration and growth-factor receptor expression
  • Cytoprotective effects in gastric and intestinal mucosa models

Primary literature

Tesamorelin

aka TH9507 · Egrifta SV

Stabilized GHRH (1-44) analogue. Stabilized GHRH analogue studied for somatotropic-axis and visceral-adiposity research.

Tesamorelin is a stabilized synthetic GHRH(1–44) analogue first characterized as TH9507. The N-terminal modification dramatically extends plasma half-life relative to native GHRH, enabling reproducible somatotropic-axis stimulation in research protocols.

Tesamorelin has been most heavily studied for its effects on the GH/IGF-1 axis and on visceral adipose tissue in HIV-associated lipodystrophy research.

Mechanism summary

Tesamorelin binds the GHRH receptor on anterior-pituitary somatotrophs, driving pulsatile release of endogenous growth hormone. Downstream:

  • GH-mediated hepatic IGF-1 synthesis
  • Lipolytic signaling at visceral adipocytes
  • Net effects on body-composition markers in published trials

Primary literature

Sermorelin

aka GRF(1-29) amide

GHRH (1-29) amide. Truncated GHRH analogue studied for pulsatile GH release and recovery-pathway research.

Sermorelin is a 29-amino-acid amide corresponding to the active N-terminal fragment of native GHRH. It retains full GHRH-receptor binding activity in a more economical, easier-to-manufacture sequence than the full 44-residue parent peptide.

Sermorelin is widely used as a research benchmark for pulsatile somatotropic-axis stimulation and is frequently studied alongside Tesamorelin and CJC-1295 as part of GHRH-class investigations.

Mechanism summary

Sermorelin binds the GHRH receptor on pituitary somatotrophs, evoking a physiologic pulse of endogenous growth hormone — preserving the body's negative-feedback architecture, unlike exogenous GH administration. Downstream effects mirror native GHRH activity.

Primary literature

MT-II

aka Melanotan II

Cyclic α-MSH analogue. Cyclic heptapeptide studied for melanocortin-receptor pathways including pigmentation and libido.

Melanotan II (MT-II) is a cyclic synthetic analogue of α-MSH (alpha-melanocyte-stimulating hormone). The lactam bridge between Asp and Lys constrains the molecule into a bioactive conformation, increasing potency and proteolytic stability relative to linear α-MSH.

MT-II is studied across the melanocortin-receptor family — pigmentation pathways via MC1R, and central libido/arousal pathways via MC3R/MC4R.

Mechanism summary

MT-II is a non-selective agonist of the melanocortin-receptor family:

  • MC1R — eumelanin synthesis in epidermal melanocytes
  • MC3R / MC4R — central appetite and sexual-behavior pathways
  • MC5R — exocrine signaling

Primary literature

MOTS-c

aka Mitochondrial-derived peptide

Mitochondrially-encoded peptide · 16 a.a.. Mitochondria-encoded peptide investigated for AMPK signaling and metabolic-resilience research.

MOTS-c is a small mitochondrially-encoded peptide derived from an open reading frame within the 12S rRNA gene. Unlike most peptides, it is translated from mitochondrial DNA — making it one of a small class of "mitochondrial-derived peptides" (MDPs) currently under longevity-research investigation.

Preclinical work has linked MOTS-c to AMPK activation, metabolic resilience, and exercise-mimetic signaling.

Mechanism summary

MOTS-c is reported to translocate from mitochondria to the nucleus under metabolic stress and to:

  • Activate the AMPK energy-sensing pathway
  • Modulate glucose-handling and insulin-sensitivity markers in pre-clinical models
  • Influence stress-response gene programs (NRF2, antioxidant response)

Primary literature

GHK-Cu

aka Copper tripeptide-1

Copper-binding tripeptide. Naturally-occurring copper tripeptide investigated for collagen, hair, and skin-repair research.

GHK-Cu (Copper tripeptide-1) is a naturally-occurring tripeptide that binds Cu²⁺ with high affinity. Plasma concentrations of GHK decline measurably with age, and the compound has been studied extensively for its role in extracellular-matrix remodeling, wound-pathway research, and dermal-collagen signaling.

Of all the peptides in this catalog, GHK-Cu has one of the longest research literatures, dating back to the 1970s.

Mechanism summary

The GHK-Cu complex is reported to influence:

  • Collagen synthesis — type I and type III collagen up-regulation in fibroblasts
  • Extracellular-matrix remodeling — modulation of MMP / TIMP balance
  • Antioxidant pathways — copper-dependent SOD activity
  • Hair-follicle research — effects on dermal-papilla cell proliferation

Primary literature

NAD+ Buffered

aka Nicotinamide adenine dinucleotide (ox.)

pH-buffered NAD+ coenzyme. pH-buffered redox cofactor investigated for mitochondrial-energy and sirtuin-pathway research.

NAD+ Buffered is a pH-stabilized formulation of nicotinamide adenine dinucleotide — a central redox coenzyme involved in nearly every catabolic pathway in human metabolism. Solvé's buffered form mitigates the well-known injection-site discomfort of acidic NAD+ preparations in research workflows.

NAD+ is studied for its role in mitochondrial-electron-transport function, sirtuin signaling, and the broader longevity literature.

Note — NAD+ is a coenzyme, not a peptide. It is included in our catalog because of its frequency in peptide-research workflows.

Mechanism summary

NAD+ functions as the universal electron acceptor in mitochondrial energy metabolism. It is also the obligate substrate for:

  • Sirtuins (SIRT1-7) — protein-deacetylase signaling, longevity-associated pathways
  • PARPs — DNA-damage repair
  • CD38 / CD157 — extracellular NAD+ catabolism

NAD+ tissue levels decline with age, motivating its inclusion in longevity-research stacks.

Primary literature

Research use only · across all guides All content in the Solvé peptide-guides library describes peer-reviewed pre-clinical and clinical research literature. It is provided for qualified-researcher review only and does not constitute medical advice, diagnosis, treatment, prescription, or cure for any disease or condition. Solvé products are sold strictly for in-vitro research by qualified researchers and are not for human or veterinary consumption.

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