PRC
Peptide Resource Center
Precision Is Not Optional
44 Research Compounds10 Categories≥98% Purity Standard

Neuropeptides & Cognitive Research

Compounds shaping the frontier of neuroscience — from anxiolytic peptides to neurotrophic complexes.

Neuropeptide≥98%

Selank (5mg)

Institute of Molecular Genetics, Russian Academy of Sciences
One of the few synthetic anxiolytic peptides with documented cytokine-modulating activity available for neurochemical research.

Developed at Moscow's Institute of Molecular Genetics, Selank represents a rational design approach to neuropeptide therapeutics—a synthetic heptapeptide built upon the immune peptide tuftsin's structural scaffold. This derivative demonstrates the rare capacity to simultaneously modulate IL-6 expression and influence monoaminergic neurotransmitter systems, bridging neuroimmune signaling in ways few compounds can. Its dual action on GABA and serotonin pathways has positioned it as a cornerstone tool in anxiety neurobiology research.

Researchers investigating the intersection of immune signaling and behavioral neuroscience find Selank indispensable. Over two decades of Russian neurochemical research have characterized its mechanism across multiple systems, making it one of the most comprehensively studied synthetic anxiolytics in contemporary neuropharmacology.

Research Applications
Anxiety model studiescognitive function researchimmune-neuro axis modulationGABAergic pathway studiesstress response mechanismscytokine regulation research
Molecular Profile
FormulaC33H57N11O9
CAS129954-34-3
MW751.9 g/mol
Handling & Storage

Store lyophilized at -20°C in sealed vial. Upon reconstitution with bacteriostatic water, maintain at 2-8°C and utilize within 30 days. Avoid freeze-thaw cycles to preserve peptide integrity.

Researchers Also Explore
Neuropeptide≥98%

Selank (10mg)

Institute of Molecular Genetics, Russian Academy of Sciences
One of the few synthetic anxiolytic peptides with documented cytokine-modulating activity available for neurochemical research.

Developed at Moscow's Institute of Molecular Genetics, Selank represents a rational design approach to neuropeptide therapeutics—a synthetic heptapeptide built upon the immune peptide tuftsin's structural scaffold. This derivative demonstrates the rare capacity to simultaneously modulate IL-6 expression and influence monoaminergic neurotransmitter systems, bridging neuroimmune signaling in ways few compounds can. Its dual action on GABA and serotonin pathways has positioned it as a cornerstone tool in anxiety neurobiology research.

Researchers investigating the intersection of immune signaling and behavioral neuroscience find Selank indispensable. Over two decades of Russian neurochemical research have characterized its mechanism across multiple systems, making it one of the most comprehensively studied synthetic anxiolytics in contemporary neuropharmacology.

Research Applications
Anxiety model studiescognitive function researchimmune-neuro axis modulationGABAergic pathway studiesstress response mechanismscytokine regulation research
Molecular Profile
FormulaC33H57N11O9
CAS129954-34-3
MW751.9 g/mol
Handling & Storage

Store lyophilized at -20°C in sealed vial. Upon reconstitution with bacteriostatic water, maintain at 2-8°C and utilize within 30 days. Avoid freeze-thaw cycles to preserve peptide integrity.

Researchers Also Explore
Neuropeptide≥98%

Semax (5mg)

Institute of Molecular Genetics, Russian Academy of Sciences
The only synthetic ACTH analogue specifically engineered to penetrate the blood-brain barrier and elevate BDNF expression.

Semax emerged from the same Moscow laboratory that produced Selank, but with an entirely different objective: augmenting cognitive capacity through neurotrophic upregulation. This heptapeptide analogue of the ACTH(4-10) fragment demonstrates a mechanism rare among small peptides—it crosses the blood-brain barrier intact and directly increases brain-derived neurotrophic factor expression in cortical and hippocampal regions. The result: enhanced neuroplasticity, improved dopaminergic and serotonergic tone, and measurable effects on memory consolidation in experimental models.

Where most nootropics rely on neurotransmitter modulation alone, Semax operates upstream—influencing the very production of proteins that govern synaptic remodeling. Its effects on cerebrovascular function have made it a staple in stroke recovery research, while cognitive neuroscientists value its ability to enhance working memory without stimulant-like side effects.

Research Applications
BDNF upregulation researchcognitive enhancement modelsneuroprotection studiescerebrovascular function researchattention and memory mechanismsstroke recovery pathways
Molecular Profile
FormulaC37H51N9O10S
CAS80714-61-0
MW813.9 g/mol
Handling & Storage

Store lyophilized at -20°C protected from light. Reconstitute with bacteriostatic or sterile water; maintain at 2-8°C and use within 30 days. This peptide exhibits enhanced stability compared to unmodified ACTH fragments.

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Neuropeptide≥98%

DSIP (5mg)

First isolated from rabbit cerebral venous blood, 1977
The original sleep-inducing peptide—a naturally occurring nonapeptide that launched the field of endogenous sleep regulation research.

Delta Sleep-Inducing Peptide represents a landmark discovery in chronobiology. Isolated from the cerebral venous blood of sleeping rabbits in 1977 by Swiss researchers Schoenenberger and Monnier, DSIP opened scientific inquiry into endogenous sleep architecture modulation. Unlike sedatives that suppress neural activity, this nonapeptide appears to facilitate natural sleep-wake transitions through circadian rhythm entrainment and stress hormone regulation.

The peptide's mechanism extends beyond simple sleep induction: it modulates stress response systems, exhibits analgesic properties in pain perception studies, and demonstrates cortisol-regulating effects that have made it valuable in neuroendocrine research. Decades of investigation have revealed DSIP's subtle, multi-system influence—acting more as a biological rhythm optimizer than a traditional sleep agent.

Research Applications
Sleep architecture studiescircadian rhythm regulationstress-response neuroendocrine pathwayspain perception modulationcortisol dynamics researchdelta wave sleep mechanisms
Molecular Profile
FormulaC35H48N10O15
CAS62568-57-4
MW848.8 g/mol
Handling & Storage

Store lyophilized at -20°C in amber vial to protect from light degradation. Upon reconstitution, store refrigerated (2-8°C) and utilize within 30 days for optimal peptide stability.

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Neuropeptide Blend≥98% (per component)

DSIP Night Blend

PRC Proprietary Formulation
A rare multi-peptide formulation combining three complementary sleep-regulating neuropeptides studied for their synergistic effects on circadian biology.

Sleep architecture involves layered neurochemical systems—GABAergic inhibition, serotonergic tone, melatonergic timing, and neuropeptide signaling all converge to orchestrate restorative sleep. This proprietary blend recognizes that complexity, combining DSIP with complementary peptides that target distinct but overlapping pathways in sleep-wake regulation. The formulation enables researchers to investigate multi-system sleep modulation in ways single-agent studies cannot capture.

Unlike crude sedative approaches, this blend mirrors the brain's endogenous sleep-promoting cascade—facilitating rather than forcing the transition to restorative sleep states. Chronobiology researchers studying circadian misalignment, sleep disorder pathophysiology, or the molecular architecture of sleep cycles find this combination invaluable for modeling natural sleep regulation.

Research Applications
Multi-peptide sleep architecture studiescircadian entrainment mechanismsneurotransmitter interaction models in sleeprestorative sleep pathway researchsleep disorder neurochemistry
Handling & Storage

Store lyophilized at -20°C protected from light and moisture. Reconstituted solution remains stable at 2-8°C for up to 30 days when stored properly. Single-use aliquoting recommended for repeated experiments.

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Neurotrophic Factor ComplexPharmaceutical grade

Cerebrolysin (60mg)

Porcine brain-derived peptide preparation, Austria
The only commercially available multi-factor neurotrophic complex that mimics endogenous brain-derived growth factors across multiple receptor systems.

Cerebrolysin stands apart in neuroprotection research: where most compounds target a single pathway, this pharmaceutical-grade preparation contains a complex mixture of low-molecular-weight neuropeptides and amino acids derived from porcine brain tissue. The result is a biological profile that simultaneously activates multiple neurotrophic signaling cascades—mimicking BDNF, NGF, CNTF, and GDNF pathways that govern neuroplasticity, cell survival, and synaptic remodeling.

Developed in Austria and extensively studied across European and Asian research institutions, Cerebrolysin has accumulated over 300 published studies in neurodegenerative disease models, stroke recovery, and traumatic brain injury research. Its mechanism—providing exogenous neurotrophic support when endogenous systems fail—makes it irreplaceable in neuroprotection studies where single-target interventions prove insufficient.

Research Applications
Multi-pathway neuroprotectionneurodegenerative disease modelspost-stroke neuroplasticitysynaptic preservation studiesneurotrophic factor signalingcognitive impairment research
Handling & Storage

Store refrigerated at 2-8°C in original sealed ampules. Do not freeze. Protect from direct light. Use immediately upon opening; this product does not contain preservatives. Stable unopened for 24 months under proper conditions.

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GLP Receptor Agonists

The molecules redefining metabolic research — single, dual, and triple receptor agonists.

GLP-1 Receptor Agonist≥98%

Semaglutide (GLP-1 Receptor Agonist)

Novo Nordisk research, Denmark
The benchmark long-acting GLP-1 receptor agonist—a fatty acid-modified peptide that redefined incretin-based metabolic research.

Semaglutide represents the culmination of decades of incretin biology research. Novo Nordisk's scientists engineered this glucagon-like peptide-1 analogue with a strategic fatty acid modification that enables albumin binding, dramatically extending its half-life from minutes to days. This single molecular modification transformed GLP-1 from a rapidly degraded hormone into a sustained metabolic signaling tool, enabling researchers to study prolonged GLP-1 receptor activation without the confounding variables of pulsatile dosing.

The compound's potency at GLP-1 receptors—combined with its resistance to DPP-4 degradation—has made it the gold standard in metabolic research models. Studies investigating glucose homeostasis, pancreatic beta-cell function, appetite regulation via hypothalamic pathways, and incretin receptor pharmacology consistently rely on semaglutide as the reference GLP-1 agonist.

Research Applications
GLP-1 receptor binding and signaling studiesglucose homeostasis mechanismspancreatic beta-cell function researchappetite regulation pathwaysincretin pharmacologymetabolic disease models
Molecular Profile
FormulaC187H291N45O59
CAS910463-68-2
MW4113.6 g/mol
Handling & Storage

Store lyophilized at -20°C protected from light. Upon reconstitution with bacteriostatic water, store at 2-8°C and use within 30 days. The acylated structure provides enhanced stability compared to native GLP-1.

Researchers Also Explore
Dual GLP-1/GIP Receptor Agonist≥98%

Tirzepatide (20mg)

Eli Lilly research, United States
The first dual incretin receptor agonist—a fusion peptide that simultaneously activates GLP-1 and GIP pathways for unprecedented metabolic effects.

Tirzepatide represents a paradigm shift in incretin biology. Where previous research focused on single-receptor agonism, Eli Lilly scientists engineered this novel peptide to activate both glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptors with balanced potency. The compound's structure—based on the native GIP sequence with modifications that confer GLP-1 activity—creates a dual agonist profile impossible to achieve with natural hormones.

This dual incretin activation reveals synergistic metabolic effects: GIP enhances insulin secretion and may support beta-cell health, while GLP-1 provides appetite suppression and delays gastric emptying. Researchers studying incretin receptor cross-talk, synergistic metabolic signaling, or the distinct contributions of GIP versus GLP-1 pathways find tirzepatide indispensable for dissecting complex incretin physiology.

Research Applications
Dual incretin pathway researchGIP/GLP-1 receptor synergyincretin receptor pharmacologymetabolic signaling cascade studiespancreatic islet functioncomparative incretin biology
Molecular Profile
FormulaC225H348N48O68
CAS2023788-19-2
MW4813.5 g/mol
Handling & Storage

Store lyophilized at -20°C in sealed container. Reconstitute with bacteriostatic water; maintain at 2-8°C for up to 30 days. The fatty acid modification provides proteolytic resistance and extended stability.

Researchers Also Explore
Dual GLP-1/GIP Receptor Agonist≥98%

Tirzepatide (30mg)

Eli Lilly research, United States
The first dual incretin receptor agonist—a fusion peptide that simultaneously activates GLP-1 and GIP pathways for unprecedented metabolic effects.

Tirzepatide represents a paradigm shift in incretin biology. Where previous research focused on single-receptor agonism, Eli Lilly scientists engineered this novel peptide to activate both glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptors with balanced potency. The compound's structure—based on the native GIP sequence with modifications that confer GLP-1 activity—creates a dual agonist profile impossible to achieve with natural hormones.

This dual incretin activation reveals synergistic metabolic effects: GIP enhances insulin secretion and may support beta-cell health, while GLP-1 provides appetite suppression and delays gastric emptying. Researchers studying incretin receptor cross-talk, synergistic metabolic signaling, or the distinct contributions of GIP versus GLP-1 pathways find tirzepatide indispensable for dissecting complex incretin physiology.

Research Applications
Dual incretin pathway researchGIP/GLP-1 receptor synergyincretin receptor pharmacologymetabolic signaling cascade studiespancreatic islet functioncomparative incretin biology
Molecular Profile
FormulaC225H348N48O68
CAS2023788-19-2
MW4813.5 g/mol
Handling & Storage

Store lyophilized at -20°C in sealed container. Reconstitute with bacteriostatic water; maintain at 2-8°C for up to 30 days. The fatty acid modification provides proteolytic resistance and extended stability.

Researchers Also Explore
Triple GLP-1/GIP/Glucagon Receptor Agonist≥98%

Retatrutide (20mg)

Eli Lilly research, United States
The world's first triple-agonist peptide—simultaneously activating GLP-1, GIP, and glucagon receptors to unlock metabolic effects impossible with dual agonism.

Retatrutide represents the frontier of incretin research. Building on tirzepatide's dual-agonist success, Eli Lilly scientists engineered this peptide with an unprecedented pharmacological profile: balanced activation of three distinct hormone receptors—GLP-1, GIP, and glucagon. This triple agonism creates a metabolic phenotype unattainable through any combination of existing compounds: incretin-mediated glucose regulation and appetite suppression, plus glucagon-driven energy expenditure.

The addition of glucagon receptor activity—traditionally avoided in metabolic therapies due to hyperglycemic concerns—proves synergistic when balanced with GLP-1 and GIP signaling. Researchers investigating energy balance, thermogenesis, complex metabolic pathway interactions, or next-generation incretin pharmacology find retatrutide essential for exploring multi-receptor agonism strategies.

Research Applications
Triple-receptor agonism studiesGLP-1/GIP/glucagon pathway synergyenergy expenditure mechanismscomplex metabolic signalingthermogenesis researchnext-generation incretin biology
Molecular Profile
FormulaC221H342N46O68
CAS2381089-83-2
MW4731.0 g/mol
Handling & Storage

Store lyophilized at -20°C protected from moisture. Reconstitute with bacteriostatic water; stable at 2-8°C for 30 days. Handle with care—this represents one of the most complex peptide agonists in metabolic research.

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Amylin Analogue≥98%

Cagrilintide (5mg)

Novo Nordisk research, Denmark
A next-generation amylin receptor agonist with extended half-life—enabling sustained study of amylin's role in satiety, gastric emptying, and glucose regulation.

Cagrilintide reimagines amylin pharmacology. While the first-generation amylin analogue pramlintide required frequent dosing and suffered from limited stability, Novo Nordisk's structural modifications created a compound with dramatically extended receptor residence time and proteolytic resistance. This long-acting analogue enables researchers to study sustained amylin receptor activation—revealing roles for this often-overlooked hormone in metabolic regulation that short-acting compounds cannot illuminate.

Amylin, co-secreted with insulin from pancreatic beta cells, serves as a critical satiety signal and gastric motility regulator. Cagrilintide's enhanced pharmacokinetics make it ideal for investigating amylin receptor biology, the interplay between amylin and incretin pathways, and the therapeutic potential of sustained amylin agonism in metabolic disease models.

Research Applications
Amylin receptor signaling researchgastric emptying mechanismssatiety pathway studiespancreatic beta-cell co-secretionpramlintide comparison pharmacologycalcitonin receptor family research
Molecular Profile
FormulaC194H312N54O59S2
CAS2374769-38-1
MW4409.5 g/mol
Handling & Storage

Store lyophilized at -20°C in sealed vial. Upon reconstitution, maintain refrigerated at 2-8°C and use within 30 days. The acylated structure provides exceptional stability compared to native amylin.

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Growth Hormone Secretagogues

Precision tools for studying the GH axis — from GHRH analogues to ghrelin receptor agonists.

Growth Hormone Releasing Hormone Analogue≥98%

Sermorelin (5mg)

United States pharmaceutical development
The truncated yet fully bioactive fragment of human GHRH—a 29-amino acid sequence that retains complete growth hormone releasing activity.

Sermorelin represents elegant peptide design: by identifying the minimal bioactive sequence within full-length GHRH(1-44), researchers created a compound with identical receptor activity but enhanced stability and reduced immunogenicity. This 29-amino acid fragment contains the entire receptor-binding domain, making it indispensable for studying GHRH receptor pharmacology without the complications of the full 44-residue hormone.

The peptide binds selectively to GHRH receptors on pituitary somatotrophs, triggering endogenous growth hormone release through natural pulsatile mechanisms. Unlike exogenous growth hormone administration, sermorelin preserves the physiological feedback loops governing GH secretion, making it the preferred tool for studying growth hormone axis regulation, pituitary function, and the upstream control of IGF-1 production.

Research Applications
GHRH receptor binding studiespituitary somatotroph functiongrowth hormone secretion dynamicspulsatile GH release mechanismsIGF-1 pathway researchgrowth hormone axis physiology
Molecular Profile
FormulaC149H246N44O42S
CAS86168-78-7
MW3357.9 g/mol
Handling & Storage

Store lyophilized at -20°C protected from light. Reconstitute with bacteriostatic water; maintain at 2-8°C and use within 30 days. The truncated structure provides improved stability versus full-length GHRH.

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Growth Hormone Secretagogue≥98%

Ipamorelin (5mg)

Novo Nordisk research, Denmark
The most selective growth hormone secretagogue available—a pentapeptide with exceptional specificity for GH release without prolactin or cortisol elevation.

Ipamorelin solved a critical problem in growth hormone secretagogue research: earlier ghrelin mimetics like GHRP-6 and GHRP-2 stimulated GH release but also elevated prolactin and cortisol through off-target receptor activation. Novo Nordisk's Ipamorelin, a carefully designed pentapeptide, demonstrates near-exclusive selectivity for the ghrelin receptor (GHS-R1a) on somatotrophs, triggering GH secretion without the hormonal side effects that confound experimental interpretation.

This selectivity makes ipamorelin the gold standard for dissecting ghrelin receptor pharmacology and GH secretion mechanisms. Researchers studying the distinction between GHRH-mediated and ghrelin-mediated GH release, or investigating selective GH secretagogue approaches, find this peptide essential for clean, interpretable results.

Research Applications
Ghrelin receptor (GHS-R1a) pharmacologyselective GH secretion mechanismsgrowth hormone pulse dynamicssomatotroph receptor selectivityGHRP comparative studiesnon-GHRH secretagogue pathways
Molecular Profile
FormulaC38H49N9O5
CAS170851-70-4
MW711.9 g/mol
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution with bacteriostatic water, refrigerate at 2-8°C and utilize within 30 days. Ipamorelin demonstrates excellent stability in solution compared to earlier secretagogues.

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Growth Hormone Releasing Hormone Analogue≥98%

CJC-1295 no DAC (5mg)

Modified GHRH research, United States
A strategically modified GHRH analogue with enhanced proteolytic resistance—offering the benefits of extended stability without the prolonged binding of DAC-conjugated versions.

CJC-1295 without Drug Affinity Complex (commonly called Modified GRF 1-29 or Mod GRF) represents refined GHRH analogue design. Through targeted amino acid substitutions at positions vulnerable to enzymatic cleavage, researchers created a peptide significantly more stable than natural GHRH yet without the week-long half-life of DAC-conjugated CJC-1295. This intermediate stability profile proves ideal for studying pulsatile GH release—the natural physiological pattern that continuous GHRH exposure would obscure.

The compound binds GHRH receptors with high affinity while resisting degradation by plasma peptidases, enabling multi-hour experimental windows without the supraphysiological, sustained activation that DAC conjugation creates. Researchers investigating natural GH pulse architecture, GHRH receptor desensitization, or physiological GH secretion patterns prefer this version for its balance of stability and pulsatility.

Research Applications
GHRH analogue pharmacologypulsatile GH release patternsGHRH receptor binding kineticspeptide stability mechanismsgrowth hormone secretion dynamicssomatotroph physiology
Molecular Profile
FormulaC165H269N47O46
CAS863288-34-0
MW3647.2 g/mol
Handling & Storage

Store lyophilized at -20°C protected from light and moisture. Reconstitute with bacteriostatic water; stable at 2-8°C for 30 days. The structural modifications provide significant proteolytic resistance.

Researchers Also Explore
Dual Growth Hormone Secretagogue≥98% (per component)

CJC-1295/Ipamorelin Combination (5mg/5mg)

Synergistic research formulation
A precision-balanced combination targeting both GHRH and ghrelin pathways—enabling investigation of synergistic GH secretion mechanisms that single agents cannot reveal.

Growth hormone release is governed by two parallel pathways: GHRH signaling through pituitary GHRH receptors, and ghrelin acting via GHS-R1a receptors. This combination recognizes that dual-pathway activation produces supra-additive effects—the GH pulse amplitude from combined GHRH/ghrelin agonism exceeds the sum of individual stimulation. The mechanism involves distinct intracellular signaling cascades that converge on GH granule release, with ghrelin potentially amplifying GHRH's effects through calcium mobilization.

Researchers studying GH secretion physiology, investigating secretagogue synergy, or modeling maximal endogenous GH release find this pre-optimized ratio invaluable. The combination eliminates dosing variables, ensuring consistent GHRH:ghrelin pathway stimulation across experiments—a critical factor in reproducible GH research.

Research Applications
Dual-pathway GH secretagogue studiesGHRH/ghrelin synergy mechanismsamplified GH pulse researchcombined secretagogue pharmacodynamicsmaximal endogenous GH release models
Handling & Storage

Store lyophilized at -20°C in sealed dual-chamber vial. Reconstitute both components simultaneously; maintain at 2-8°C and use within 30 days. Both peptides exhibit excellent co-stability in solution.

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Recombinant Human Growth Hormone≥98%

HGH 191 (1500 IU)

Recombinant E. coli expression system
Bioidentical 191-amino acid human growth hormone produced via recombinant DNA technology—the reference standard for GH receptor research.

This represents human somatotropin in its native form: 191 amino acids in the precise sequence and tertiary structure found in pituitary-derived growth hormone. Produced through recombinant DNA technology in E. coli expression systems, this rHGH is structurally indistinguishable from endogenous GH, making it the unambiguous choice for studying growth hormone receptor binding, GH-mediated signal transduction, and the direct effects of somatotropin on target tissues.

Where secretagogues provide indirect GH elevation through endogenous release, direct GH administration enables precise dose-response studies, receptor saturation experiments, and investigation of GH signaling independent of pituitary function. With over four decades of research characterizing GH's effects on IGF-1 production, lipolysis, protein synthesis, and tissue remodeling, this molecule remains central to endocrine and metabolic research.

Research Applications
GH receptor binding and signalingIGF-1 pathway researchsomatotropin receptor pharmacologyanabolic signaling mechanismsdirect GH effects vs. secretagogue comparisonprotein synthesis research
Molecular Profile
FormulaC990H1528N262O300S7
CAS12629-01-5
MW22,124 g/mol
Handling & Storage

Store lyophilized at -20°C protected from light. Upon reconstitution with bacteriostatic water, maintain at 2-8°C and use within 14 days—shorter than peptide secretagogues due to protein aggregation susceptibility. Avoid agitation; gently swirl to dissolve.

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Tissue Repair & Regeneration

The repair toolkit — peptides that drive angiogenesis, cell migration, and tissue remodeling.

Tissue Repair Peptide Complex≥98% (per component)

BPC-157/TB-500 Combination (10mg/10mg)

Synergistic research formulation
The most widely researched tissue repair combination—pairing BPC-157's cytoprotective mechanisms with TB-500's actin-mediated cell migration for comprehensive healing studies.

Tissue repair requires coordinated processes: inflammatory resolution, angiogenesis, cell migration, extracellular matrix remodeling, and cytoprotection. This combination targets multiple phases simultaneously. BPC-157, a pentadecapeptide partial sequence of the body protection compound isolated from gastric juice, demonstrates remarkable cytoprotective properties in mucosal tissue while promoting angiogenesis through VEGF modulation. TB-500 (Thymosin Beta-4 fragment) facilitates actin polymerization and cytoskeletal reorganization, driving cell migration to injury sites and promoting extracellular matrix formation.

Their mechanisms complement: BPC-157 protects existing tissue and stimulates new vessel formation, while TB-500 mobilizes repair cells and promotes structural regeneration. With hundreds of published studies investigating each peptide individually, researchers increasingly combine them to model multi-phase tissue healing—from acute injury response through complete structural restoration.

Research Applications
Wound healing modelsangiogenesis researchcytoprotection mechanismscell migration assayscollagen synthesis studiesanti-inflammatory pathway researchmusculoskeletal repair models
Handling & Storage

Store lyophilized at -20°C protected from moisture. Both peptides remain stable when co-reconstituted; maintain at 2-8°C and use within 30 days. Compatible in the same solution without interaction.

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Anti-inflammatory Tripeptide≥98%

KPV (10mg)

C-terminal fragment of α-MSH
The isolated anti-inflammatory domain of α-MSH—a tripeptide that retains potent NF-κB inhibition without melanocortin receptor activation.

KPV (Lysine-Proline-Valine) represents molecular dissection of anti-inflammatory signaling. As the C-terminal tripeptide of alpha-melanocyte stimulating hormone, KPV retains the parent molecule's remarkable anti-inflammatory properties while eliminating melanocortin receptor-mediated effects like pigmentation. This separation of functions makes KPV uniquely valuable: it modulates inflammatory gene transcription through NF-κB pathway inhibition and reduces pro-inflammatory cytokine production without the broader melanocortin system effects.

Research has demonstrated KPV's effectiveness in inflammatory bowel disease models, dermal inflammation studies, and wound healing research where inflammation must be controlled without suppressing the entire immune response. Its ability to penetrate epithelial barriers and concentrate in inflamed tissues makes it particularly relevant for mucosal inflammation research.

Research Applications
NF-κB signaling inhibitioninflammatory cytokine modulationinflammatory bowel disease modelsmucosal immunity researchwound healing inflammation controlmelanocortin peptide fragment studies
Molecular Profile
FormulaC16H30N4O4
CAS61090-95-7
MW342.4 g/mol
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution with bacteriostatic water, maintain at 2-8°C and use within 30 days. This small peptide demonstrates excellent stability in solution.

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Copper Peptide Complex≥98%

GHK-Cu (100mg)

Naturally occurring tripeptide, first isolated from human plasma
The archetypal copper-peptide complex—a naturally occurring tripeptide that chelates Cu²⁺ to modulate metalloproteinases, collagen synthesis, and tissue remodeling.

Glycyl-L-Histidyl-L-Lysine bound to copper represents one of nature's elegant metal-mediated signaling systems. First isolated from human plasma in the 1970s by Dr. Loren Pickart, GHK-Cu demonstrates the biological importance of copper-peptide coordination chemistry. The copper ion, precisely positioned by the peptide's histidine and terminal amine, activates the complex's biological functions: stimulating collagen and glycosaminoglycan synthesis, modulating metalloproteinase activity for balanced extracellular matrix remodeling, and providing localized antioxidant effects.

GHK-Cu's plasma concentration declines with age, correlating with diminished tissue repair capacity—a relationship that has driven extensive research into its role in wound healing, dermal remodeling, and tissue regeneration. The peptide's ability to simultaneously promote matrix synthesis and regulate degradation makes it irreplaceable in studies of balanced tissue remodeling.

Research Applications
Collagen synthesis mechanismsmetalloproteinase regulationcopper-dependent enzyme researchextracellular matrix remodelingwound healing biologyantioxidant copper chemistrytissue regeneration models
Molecular Profile
FormulaC14H24N6O4·Cu
CAS49557-75-7
MW404.0 g/mol
Handling & Storage

Store lyophilized at -20°C protected from light (copper complexes are photosensitive). Reconstitute with sterile water; the copper complex remains stable at 2-8°C for 30 days. Avoid oxidizing agents.

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Antimicrobial Peptide≥98%

LL-37 (5mg)

Human cathelicidin hCAP18, cleaved C-terminal fragment
The sole human cathelicidin—a 37-amino acid amphipathic peptide representing the first line of innate immune defense against pathogens.

LL-37 occupies a unique position in human immunology: it is the only antimicrobial peptide produced by the human cathelicidin family, unlike other species that express multiple cathelicidin variants. Cleaved from the C-terminus of the hCAP18 precursor protein, this amphipathic alpha-helical peptide demonstrates broad-spectrum antimicrobial activity against bacteria, fungi, and enveloped viruses through membrane disruption. Beyond direct antimicrobial action, LL-37 exhibits immunomodulatory functions—recruiting immune cells, modulating inflammatory responses, and promoting wound closure.

Expression of LL-37 is induced by vitamin D, linking nutritional status to innate immune capacity—a relationship that has made this peptide central to research on vitamin D-dependent immunity. Its multi-functional profile (antimicrobial, chemotactic, angiogenic, and wound-healing) makes LL-37 essential for studying the complex roles of antimicrobial peptides beyond simple pathogen killing.

Research Applications
Antimicrobial mechanism studiesinnate immunity researchmembrane disruption modelsbiofilm penetration researchimmune cell chemotaxiswound healing immunityvitamin D-dependent peptide regulation
Molecular Profile
FormulaC205H340N60O53
CAS154947-66-7
MW4493.3 g/mol
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution, maintain at 2-8°C and use within 30 days. The amphipathic structure requires gentle handling to prevent aggregation at higher concentrations.

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Thymic Bioregulator≥98%

Thymalin (10mg)

Bovine thymus gland extract, Russia
A pharmaceutical-grade thymic extract representing the bioregulator class—short peptides that modulate organ-specific cellular function through epigenetic mechanisms.

Thymalin belongs to a unique category of biological compounds developed in the Soviet Union: bioregulators—short peptides (typically 2-4 amino acids) extracted from specific organs that demonstrate tissue-specific regulatory effects. Isolated from thymus tissue, Thymalin contains peptides that appear to modulate T-cell differentiation and thymic function through mechanisms still being elucidated, possibly involving chromatin remodeling and gene expression regulation.

The bioregulator hypothesis suggests these short peptides bind to DNA regulatory regions, influencing cell differentiation and function in their tissue of origin. While mechanistic details continue to emerge, decades of research in Russia and Eastern Europe have characterized Thymalin's effects on immune function, T-cell populations, and adaptive immunity—making it valuable for thymic biology research and immunosenescence studies.

Research Applications
T-cell differentiation studiesthymic function researchbioregulator peptide mechanismsimmune system modulationimmunosenescence modelsadaptive immunity researchpeptide-DNA interaction studies
Handling & Storage

Store lyophilized at -20°C protected from moisture. Reconstitute with sterile or bacteriostatic water; maintain at 2-8°C and use within 30 days. As a biological extract, handle with standard peptide precautions.

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Biological ExtractPharmaceutical grade

Laennec Ampules (Human Placental Extract)

Human placenta, Japan pharmaceutical manufacture
A pharmaceutical-grade human placental hydrolysate containing over 50 identified growth factors—the most complex multi-factor biological preparation available for regenerative research.

Laennec represents the biological complexity that single-molecule research cannot capture. This pharmaceutical-grade extract, derived from healthy human placenta and manufactured under strict Japanese pharmaceutical standards, contains a remarkably diverse array of bioactive molecules: multiple growth factor families (FGF, EGF, VEGF, HGF), cytokines, amino acids, vitamins, and minerals that collectively drive tissue regeneration. The placenta—nature's most rapidly growing temporary organ—concentrates factors that promote cell proliferation, angiogenesis, and tissue remodeling.

Unlike recombinant single-factor preparations, Laennec provides the factor combinations and ratios that occur naturally during development and healing. Researchers studying complex tissue regeneration, investigating growth factor synergies, or modeling multi-factor biological environments find this extract invaluable for capturing biological complexity that simplified systems miss.

Research Applications
Multi-growth factor signalingtissue regeneration modelscytokine interaction studiescomplex biological system researchangiogenesis with multiple factorscellular metabolism in growth factor-rich environments
Handling & Storage

Store refrigerated at 2-8°C in sealed ampules. Do not freeze—freezing damages the biological factor profile. Protect from direct light. Use immediately upon opening; no preservatives present. Stable 24 months unopened under proper refrigeration.

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Metabolic Research Compounds

From mitochondrial-derived peptides to lipotropic blends — every metabolic pathway covered.

Modified Growth Hormone Fragment≥98%

AOD-9604 (2mg)

Monash University, Australia
A strategically modified fragment of growth hormone's C-terminus—retaining lipolytic activity while eliminating GH receptor activation and IGF-1 elevation.

AOD-9604 (Advanced Obesity Drug) represents molecular surgery on growth hormone. Australian researchers at Monash University identified the 176-191 C-terminal region as responsible for GH's lipolytic effects, then added stabilizing modifications to create a fragment that stimulates lipolysis without growth hormone receptor binding. The result: a peptide that mimics GH's fat-mobilizing properties while completely avoiding effects on growth, glucose metabolism, or IGF-1—a clean separation impossible with full-length GH.

This selective action makes AOD-9604 invaluable for dissecting GH's metabolic effects. Researchers can investigate lipolytic signaling mechanisms, study adipocyte beta-oxidation, and explore growth hormone's metabolic functions without the confounding variables of receptor-mediated GH actions. The fragment's mechanism—potentially involving non-receptor-mediated pathways—remains an active area of investigation.

Research Applications
Lipolysis mechanism researchGH fragment biologylipid metabolism studiesadipocyte signaling independent of GH receptorselective metabolic pathway activationnon-receptor GH effects
Molecular Profile
FormulaC78H123N23O23S2
CAS221231-10-3
MW1815.1 g/mol
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution with bacteriostatic water, maintain at 2-8°C and use within 30 days. The modifications provide enhanced stability compared to unmodified HGH fragments.

Researchers Also Explore
Mitochondrial-Derived Peptide≥98%

MOTS-c (10mg)

USC Leonard Davis School of Gerontology
The first identified mitochondrial open reading frame-encoded peptide—a 16-amino acid sequence that translocates to the nucleus to regulate metabolism.

MOTS-c represents a paradigm shift in cellular biology. Discovered in 2015 by researchers at USC, this peptide revealed that the mitochondrial genome—long thought to encode only 13 proteins—contains open reading frames for signaling peptides that regulate nuclear gene expression. MOTS-c, encoded within the mitochondrial 12S rRNA gene, acts as a mitochondrial-to-nuclear messenger: during metabolic stress, it translocates to the nucleus and binds DNA regulatory regions, modulating expression of genes involved in glucose metabolism and insulin sensitivity.

This mitochondrial-nuclear communication pathway challenges traditional views of metabolic regulation. MOTS-c activates AMPK, enhances glucose uptake, and improves metabolic flexibility—effects that position it at the intersection of aging research, metabolic disease modeling, and the study of retrograde signaling from mitochondria to nucleus.

Research Applications
Mitochondrial-nuclear signalingmetabolic homeostasis mechanismsAMPK pathway researchinsulin sensitivity studiesmitochondrial genome functionretrograde signaling researchexercise mimetic studies
Molecular Profile
FormulaC101H152N28O22S2
CAS1627580-64-6
MW2174.6 g/mol
Handling & Storage

Store lyophilized at -20°C protected from moisture. Reconstitute with bacteriostatic water; stable at 2-8°C for 30 days. Handle as a standard peptide despite its mitochondrial origin.

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NNMT Inhibitor≥98%

5-Amino-1MQ (5mg)

Small molecule research compound
A selective small molecule inhibitor of nicotinamide N-methyltransferase—increasing cellular NAD+ availability through enzymatic blockade of the methylation pathway.

5-Amino-1-methylquinolinium targets a metabolic bottleneck: nicotinamide N-methyltransferase (NNMT), an enzyme that consumes NAD+ precursors by methylating nicotinamide for excretion. By inhibiting NNMT, 5-Amino-1MQ preserves intracellular nicotinamide, allowing its recycling back to NAD+ through the salvage pathway. This mechanism provides an alternative approach to NAD+ augmentation—rather than supplying more precursor, block the pathway that depletes it.

NNMT overexpression correlates with metabolic dysfunction and adiposity in preclinical models, suggesting this enzyme represents a metabolic control point. Research with 5-Amino-1MQ explores NNMT's role in NAD+ homeostasis, methylation reactions, energy metabolism, and the enzyme's potential as a metabolic regulatory target. Note: This is an oral small molecule, not an Liquid Reagent peptide.

Molecular Profile
FormulaC10H11N2+
CAS42464-96-0
MW159.2 g/mol
Handling & Storage

Store at room temperature (15-30°C) in sealed container protected from moisture. This small molecule exhibits excellent stability. For research use, dissolve in appropriate vehicle according to experimental protocol.

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Metabolic Research Blend≥98% (per component)

Lipo-C MAX Blend

PRC formulation
A precision-formulated lipotropic blend combining methionine, inositol, choline, and L-carnitine—the foundational "MIC" factors that support hepatic lipid metabolism research.

The Lipo-C MAX formulation recognizes that lipid metabolism requires multiple cofactors working in concert. Methionine provides the methyl groups essential for phosphatidylcholine synthesis and methylation reactions. Inositol participates in lipid messenger signaling and cell membrane formation. Choline serves as a precursor for phosphatidylcholine and prevents hepatic lipid accumulation. L-carnitine shuttles long-chain fatty acids into mitochondria for beta-oxidation. Together, these lipotropic factors create the biochemical environment for efficient hepatic lipid processing.

Researchers studying hepatic steatosis models, investigating lipotropic factor deficiencies, or exploring the interplay between methylation and lipid metabolism find this standardized combination valuable for consistent multi-factor supplementation. The blend enables study of synergistic lipotropic mechanisms that isolated factor research cannot reveal.

Research Applications
Lipotropic factor researchhepatic lipid metabolismmethyl donor biologycholine metabolismmitochondrial fatty acid transportone-carbon metabolismphospholipid synthesis studies
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution, maintain at 2-8°C and use within 30 days. All components remain stable when combined in solution.

Researchers Also Explore
Amino Acid Derivative≥98%

L-Carnitine (600mg)

Biosynthesized from lysine and methionine
The essential cofactor for mitochondrial fatty acid oxidation—a quaternary ammonium compound that shuttles long-chain fatty acids across the impermeable inner mitochondrial membrane.

L-Carnitine (β-hydroxy-γ-trimethylaminobutyric acid) solves a fundamental problem in cellular energetics: long-chain fatty acids cannot cross the inner mitochondrial membrane where beta-oxidation occurs. Carnitine serves as the shuttle—the carnitine palmitoyltransferase (CPT) system conjugates fatty acids to carnitine, transports them across the membrane, then releases them inside the mitochondrial matrix. Without adequate carnitine, long-chain fatty acids cannot be oxidized for energy, regardless of other metabolic factors.

This bottleneck role makes L-carnitine fundamental to metabolic research. Studies of mitochondrial fatty acid oxidation, investigation of the carnitine shuttle mechanism, research into acyl-carnitine species as metabolic biomarkers, and exploration of carnitine's role in various metabolic states all require this essential cofactor.

Research Applications
Mitochondrial fatty acid transportbeta-oxidation mechanismscarnitine shuttle system researchacyl-carnitine metabolismenergy substrate utilizationmitochondrial function studiescarnitine deficiency models
Molecular Profile
FormulaC7H15NO3
CAS541-15-1
MW161.2 g/mol
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution with bacteriostatic water or sterile water, refrigerate at 2-8°C and use within 30 days. L-Carnitine demonstrates excellent solution stability.

Researchers Also Explore
Multi-Component Metabolic Blend≥98% (per component)

Lipo-C Plus Blend

PRC enhanced formulation
An advanced metabolic research formulation extending beyond basic lipotropic factors—incorporating amino acids and cofactors for comprehensive cellular energy metabolism studies.

Building upon the foundation of methionine, inositol, choline, and L-carnitine, the Lipo-C Plus formulation adds complementary factors that participate in energy production, mitochondrial function, and metabolic performance. This enhanced blend recognizes that optimal cellular metabolism requires not just lipid processing factors, but also amino acids for protein synthesis, cofactors for enzymatic reactions, and compounds that support mitochondrial efficiency.

The formulation enables researchers to investigate integrated metabolic responses—how lipotropic factors, amino acids, and energy cofactors interact to influence overall cellular bioenergetics. Studies of performance metabolism, research into multi-pathway metabolic optimization, and investigation of synergistic cofactor effects benefit from this comprehensive approach.

Research Applications
Integrated metabolic pathway researchcellular bioenergeticsmulti-cofactor synergyperformance metabolism modelsenergy production mechanismscomprehensive metabolic support systems
Handling & Storage

Store lyophilized at -20°C protected from moisture. Upon reconstitution, maintain at 2-8°C and use within 30 days. All components demonstrate co-stability in solution.

Researchers Also Explore
Premium Metabolic Research Blend≥98% (per component)

Lipo-C Ultra Blend

PRC premium formulation
The most comprehensive metabolic research formulation available—a premium blend combining lipotropic factors, amino acids, performance compounds, and mitochondrial cofactors for complete metabolic pathway coverage.

Lipo-C Ultra represents the apex of multi-component metabolic formulation. This premium blend incorporates every category of metabolic support compound: classic lipotropic factors for hepatic lipid processing, amino acids for protein synthesis and neurotransmitter production, mitochondrial cofactors for energy production, and performance-enhancing compounds for cellular optimization. The result: a research tool that enables investigation of fully-supported metabolic systems rather than isolated pathways.

Researchers exploring maximal metabolic capacity, investigating how multiple metabolic pathways integrate under optimal conditions, or studying comprehensive metabolic interventions find this formulation essential. The blend eliminates the limitation of single-factor studies, revealing system-level metabolic responses that emerge only when all necessary cofactors and substrates are available.

Research Applications
Comprehensive metabolic system researchmulti-pathway integration studiesmaximal metabolic capacity modelssystem-level bioenergeticsperformance optimization researchcomplex metabolic phenotyping
Handling & Storage

Store lyophilized at -20°C in sealed container with desiccant. Upon reconstitution, maintain at 2-8°C and use within 30 days. Despite complexity, all components maintain stability in combined solution.

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Antioxidants & Cellular Health

Cellular defense compounds — NAD+ cofactors, glutathione systems, and mitochondrial protectors.

Cellular Cofactor≥98%

NAD+ (500mg)

Biosynthetic production
The central redox cofactor in all living cells—a pyridine nucleotide essential for over 500 enzymatic reactions governing energy metabolism, DNA repair, and cellular signaling.

Nicotinamide adenine dinucleotide occupies a position of unparalleled importance in cellular biochemistry. This dinucleotide serves simultaneously as an electron carrier in redox reactions (the NAD+/NADH couple drives glycolysis, the TCA cycle, and oxidative phosphorylation), a substrate for sirtuins (deacetylases that regulate metabolism and longevity pathways), a substrate for PARPs (DNA repair enzymes), and a precursor for calcium signaling molecules. Without adequate NAD+, cellular energy production, gene expression regulation, and DNA maintenance all collapse.

NAD+ levels decline with age across tissues, correlating with metabolic dysfunction and cellular senescence—a relationship that has positioned NAD+ at the center of aging research. Studies investigating sirtuins, researching cellular energy metabolism, exploring DNA repair mechanisms, or modeling age-related NAD+ decline require direct NAD+ administration or measurement.

Research Applications
Redox biochemistrysirtuin activation researchcellular energy metabolismPARP enzyme functionmitochondrial studiesNAD+/NADH ratio measurementcellular aging mechanismsDNA repair pathways
Molecular Profile
FormulaC21H27N7O14P2
CAS53-84-9
MW663.4 g/mol
Handling & Storage

Store lyophilized at -20°C protected from light (NAD+ is photosensitive). Upon reconstitution with sterile water, use immediately or store at 2-8°C for up to 30 days. Avoid repeated freeze-thaw cycles which degrade the dinucleotide.

Researchers Also Explore
Cellular Cofactor≥98%

NAD+ (1000mg)

Biosynthetic production
The central redox cofactor in all living cells—a pyridine nucleotide essential for over 500 enzymatic reactions governing energy metabolism, DNA repair, and cellular signaling.

Nicotinamide adenine dinucleotide occupies a position of unparalleled importance in cellular biochemistry. This dinucleotide serves simultaneously as an electron carrier in redox reactions (the NAD+/NADH couple drives glycolysis, the TCA cycle, and oxidative phosphorylation), a substrate for sirtuins (deacetylases that regulate metabolism and longevity pathways), a substrate for PARPs (DNA repair enzymes), and a precursor for calcium signaling molecules. Without adequate NAD+, cellular energy production, gene expression regulation, and DNA maintenance all collapse.

NAD+ levels decline with age across tissues, correlating with metabolic dysfunction and cellular senescence—a relationship that has positioned NAD+ at the center of aging research. Studies investigating sirtuins, researching cellular energy metabolism, exploring DNA repair mechanisms, or modeling age-related NAD+ decline require direct NAD+ administration or measurement.

Research Applications
Redox biochemistrysirtuin activation researchcellular energy metabolismPARP enzyme functionmitochondrial studiesNAD+/NADH ratio measurementcellular aging mechanismsDNA repair pathways
Molecular Profile
FormulaC21H27N7O14P2
CAS53-84-9
MW663.4 g/mol
Handling & Storage

Store lyophilized at -20°C protected from light (NAD+ is photosensitive). Upon reconstitution with sterile water, use immediately or store at 2-8°C for up to 30 days. Avoid repeated freeze-thaw cycles which degrade the dinucleotide.

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Antioxidant TripeptidePharmaceutical grade

Glutathione (1200mg) - Korean Pharmaceutical Grade (10 vials)

Korea pharmaceutical manufacture
The cell's master antioxidant—a thiol-containing tripeptide that serves as the primary reducing agent, maintains redox homeostasis, and detoxifies xenobiotics across all mammalian tissues.

Glutathione (γ-L-glutamyl-L-cysteinyl-glycine) represents the first line of antioxidant defense. This tripeptide, present in millimolar concentrations in cells, functions as the primary reducing agent that neutralizes reactive oxygen species before they damage proteins, lipids, or DNA. The peptide's cysteine thiol group (-SH) provides the reducing power—glutathione oscillates between reduced (GSH) and oxidized (GSSG) forms, with the GSH/GSSG ratio serving as a key indicator of cellular redox status.

Beyond direct antioxidant action, glutathione serves as a cofactor for glutathione peroxidases (which reduce hydrogen peroxide) and glutathione S-transferases (which detoxify electrophilic compounds and xenobiotics). Manufactured in Korea to pharmaceutical standards, this preparation provides research-grade glutathione for oxidative stress studies, redox biology research, and investigation of the glutathione system's central role in cellular protection.

Research Applications
Redox biologyoxidative stress modelsglutathione peroxidase studiescellular detoxification pathwaysthiol biochemistryxenobiotic metabolismGSH/GSSG ratio studiesantioxidant defense mechanisms
Molecular Profile
FormulaC10H17N3O6S
CAS70-18-8
MW307.3 g/mol
Handling & Storage

Store refrigerated at 2-8°C in sealed pharmaceutical vials. After opening, use immediately or maintain at 2-8°C for up to 7 days. This pharmaceutical preparation is formulated for immediate research use.

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Antioxidant Tripeptide≥98%

Glutathione (1500mg)

Biosynthetic production
The cell's master antioxidant—a thiol-containing tripeptide that serves as the primary reducing agent, maintains redox homeostasis, and detoxifies xenobiotics across all mammalian tissues.

Glutathione (γ-L-glutamyl-L-cysteinyl-glycine) represents the first line of antioxidant defense. This tripeptide, present in millimolar concentrations in cells, functions as the primary reducing agent that neutralizes reactive oxygen species before they damage proteins, lipids, or DNA. The peptide's cysteine thiol group (-SH) provides the reducing power—glutathione oscillates between reduced (GSH) and oxidized (GSSG) forms, with the GSH/GSSG ratio serving as a key indicator of cellular redox status.

Beyond direct antioxidant action, glutathione serves as a cofactor for glutathione peroxidases (which reduce hydrogen peroxide) and glutathione S-transferases (which detoxify electrophilic compounds and xenobiotics). This higher-dose preparation enables concentration-dependent studies and research requiring substantial glutathione supplementation in experimental models.

Research Applications
Redox biologyoxidative stress modelsglutathione peroxidase studiescellular detoxification pathwaysthiol biochemistryxenobiotic metabolismGSH/GSSG ratio studiesantioxidant defense mechanisms
Molecular Profile
FormulaC10H17N3O6S
CAS70-18-8
MW307.3 g/mol
Handling & Storage

Store lyophilized at -20°C protected from light and oxidizing conditions. Upon reconstitution with sterile water, use promptly or store at 2-8°C for up to 30 days. Glutathione oxidizes over time; fresh solutions provide optimal reducing capacity.

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Antioxidant Cofactor≥98%

Thioctic Acid (Alpha-Lipoic Acid) (25mg/5ml)

Biosynthetic production
The only antioxidant that functions in both aqueous and lipid environments—a dithiol cofactor essential for mitochondrial energy metabolism and capable of regenerating other antioxidants.

Alpha-lipoic acid (1,2-dithiolane-3-pentanoic acid) occupies a unique position in antioxidant biology: its amphipathic structure allows it to scavenge reactive species in both water-soluble compartments (cytoplasm) and lipid-rich environments (membranes)—a property no other antioxidant possesses. Beyond direct free radical neutralization, lipoic acid serves as an essential cofactor for mitochondrial α-ketoacid dehydrogenase complexes (pyruvate dehydrogenase, α-ketoglutarate dehydrogenase), linking its antioxidant function directly to energy metabolism.

The reduced form (dihydrolipoic acid) demonstrates remarkable antioxidant activity, directly scavenging reactive oxygen and nitrogen species while regenerating other antioxidants—reducing oxidized vitamin C, vitamin E, and glutathione back to their active forms. This antioxidant network amplification makes lipoic acid a force multiplier in cellular antioxidant defense.

Research Applications
Mitochondrial cofactor functionuniversal antioxidant mechanismsantioxidant regeneration studiesglucose metabolism researchneuroprotection modelsmetal chelation researchredox signaling pathways
Molecular Profile
FormulaC8H14O2S2
CAS1077-28-7
MW206.3 g/mol
Handling & Storage

Store refrigerated at 2-8°C protected from light (light-sensitive). Supplied in solution for immediate use. Maintain sealed until use; utilize within 30 days after opening. Protect from oxidizing conditions.

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Water-Soluble AntioxidantPharmaceutical grade

Vitamin C (Ascorbic Acid) (10mg/20ml)

Pharmaceutical manufacture
The essential water-soluble antioxidant and enzymatic cofactor—a powerful reducing agent required for collagen synthesis, neurotransmitter production, and immune cell function.

L-Ascorbic acid (vitamin C) serves multiple critical biochemical roles beyond its well-known antioxidant function. As a cofactor for prolyl and lysyl hydroxylases, ascorbate is absolutely required for collagen triple helix stability—without adequate vitamin C, collagen synthesis fails, manifesting as scurvy. The vitamin also serves as cofactor for dopamine β-hydroxylase (converting dopamine to norepinephrine) and other copper-containing monooxygenases essential for neurotransmitter synthesis.

As an antioxidant, ascorbate directly reduces reactive oxygen species and serves as the first line of defense in aqueous environments. It functions synergistically with vitamin E by reducing tocopheroxyl radicals back to active tocopherol, linking water-soluble and lipid-soluble antioxidant systems. This pharmaceutical-grade Liquid Reagent preparation enables precise dosing in controlled research applications.

Research Applications
Collagen hydroxylation researchascorbate-dependent enzyme studiesantioxidant mechanism researchiron metabolismneurotransmitter synthesis pathwaysimmune cell function studiesvitamin C-dependent biochemistry
Molecular Profile
FormulaC6H8O6
CAS50-81-7
MW176.1 g/mol
Handling & Storage

Store refrigerated at 2-8°C protected from light (photosensitive). Use within 14 days after opening. Ascorbic acid oxidizes in solution over time; fresh preparations provide optimal activity. Do not freeze.

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Mitochondria-Targeting Peptide≥98%

SS-31 (Elamipretide) (10mg)

Stealth BioTherapeutics research, United States
The first peptide to selectively target and protect the inner mitochondrial membrane—an aromatic-cationic tetrapeptide that binds cardiolipin to stabilize cristae structure and reduce ROS production.

SS-31 (Szeto-Schiller peptide 31, D-Arg-Dmt-Lys-Phe-NH2) represents a breakthrough in mitochondria-targeted therapeutics. This cell-permeable tetrapeptide contains alternating cationic and aromatic residues that enable it to penetrate cells and selectively accumulate at the inner mitochondrial membrane, where it binds with high affinity to cardiolipin—the signature phospholipid of mitochondrial membranes. This cardiolipin interaction stabilizes cristae architecture, the elaborately folded inner membrane structures that house the electron transport chain.

Unlike broad antioxidants, SS-31 concentrates precisely where mitochondrial ROS are generated—at the electron transport chain. By optimizing cristae structure and reducing electron leak, SS-31 decreases reactive oxygen species production at the source while preserving mitochondrial membrane potential and ATP synthesis. This mechanism has made SS-31 invaluable in ischemia-reperfusion research, neurodegenerative disease models, and studies of mitochondrial dysfunction.

Research Applications
Mitochondrial membrane researchcardiolipin interaction studiescristae structure biologymitochondrial ROS modulationischemia-reperfusion modelsmitochondrial bioenergeticstargeted mitochondrial protection
Molecular Profile
FormulaC32H49N9O5
CAS736992-21-5
MW639.8 g/mol
Handling & Storage

Store lyophilized at -20°C protected from light. Upon reconstitution with bacteriostatic water, maintain at 2-8°C and use within 30 days. The aromatic-cationic structure provides excellent peptide stability.

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Senolytic & Longevity Research

The longevity frontier — senescent cell clearance, telomerase modulation, and neuroprotection.

Senolytic Peptide≥98%

FOXO4-DRI (10mg)

Erasmus Medical Center, Netherlands
The first peptide-based senolytic—a D-retro-inverso modified sequence that selectively disrupts the FOXO4-p53 interaction in senescent cells, triggering their apoptotic elimination.

FOXO4-DRI represents molecular precision in anti-aging research. Senescent cells—aged cells that cease dividing but resist apoptosis—accumulate with age and secrete inflammatory factors (the senescence-associated secretory phenotype, SASP) that damage surrounding tissues. Dutch researchers discovered that in senescent cells, FOXO4 protein binds and sequesters p53, preventing p53-mediated apoptosis. FOXO4-DRI, a peptide mimicking the p53-binding domain of FOXO4, competitively disrupts this interaction—freeing p53 to trigger apoptosis specifically in senescent cells.

The D-retro-inverso modification—constructing the peptide from D-amino acids in reverse sequence—creates a molecule with identical binding surface topology but dramatically enhanced proteolytic stability. This senolytic approach—selectively eliminating senescent cells while sparing healthy ones—represents a targeted strategy for addressing cellular aging.

Research Applications
Senescent cell biologyFOXO4-p53 interaction studiessenolytic mechanism researchcellular aging modelsapoptosis pathway researchSASP modulationtargeted cellular aging interventions
Molecular Profile
CAS1639871-79-4
MW~5,040 g/mol (varies by synthesis)
Handling & Storage

Store lyophilized at -20°C protected from moisture. Upon reconstitution, maintain at 2-8°C and use within 30 days. D-amino acid peptides demonstrate exceptional proteolytic stability.

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Telomerase Modulator≥98%

Epithalon (50mg)

St. Petersburg Institute of Bioregulation and Gerontology, Russia
A synthetic tetrapeptide that mimics the pineal gland's epithalamin—demonstrating telomerase activation and circadian regulation in aging research models.

Epithalon (Epitalon, Ala-Glu-Asp-Gly) emerged from decades of Russian gerontology research led by Professor Vladimir Khavinson. This tetrapeptide, designed to replicate bioactive sequences from the pineal peptide epithalamin, demonstrates two remarkable properties in experimental models: activation of telomerase (the enzyme that maintains telomere length) and modulation of circadian rhythms through melatonin regulation. These dual mechanisms position Epithalon at the intersection of cellular aging and chronobiology research.

Telomeres—the protective caps on chromosome ends—shorten with each cell division, eventually triggering senescence. Telomerase can extend telomeres, but most somatic cells suppress this enzyme. Epithalon's apparent ability to transiently activate telomerase in adult tissues has driven extensive research into its mechanism and potential for studying telomere biology and cellular aging interventions.

Research Applications
Telomerase activity researchtelomere biologycircadian rhythm regulationpineal peptide researchcellular aging mechanismsmelatonin regulation studieslongevity pathway research
Molecular Profile
FormulaC14H22N4O9
CAS307297-39-8
MW390.3 g/mol
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution with bacteriostatic water, maintain at 2-8°C and use within 30 days. This short peptide demonstrates good stability in solution.

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Neuroprotective Heptapeptide≥98%

PE 22-28 (10mg)

Based on spadin research, France
A synthetic fragment of the sortilin propeptide—a heptapeptide that modulates TREK-1 potassium channels to influence neuroplasticity and neuroprotection.

PE 22-28 represents targeted neuroplasticity research. This heptapeptide, corresponding to amino acids 22-28 of the propeptide region of sortilin (a protein involved in neurotrophin sorting), was identified through research into spadin—an endogenous peptide with neuroprotective properties. PE 22-28 interacts with TREK-1 (TWIK-related potassium channel), a background potassium channel involved in neuronal excitability, synaptic plasticity, and stress response.

By modulating TREK-1 channel activity, PE 22-28 influences neuronal membrane potential and excitability, with downstream effects on neurotrophic signaling and synaptic remodeling. Research suggests this peptide may enhance neuroplasticity—the brain's capacity to reorganize synaptic connections—making it valuable for studying neuroadaptation, neuroprotection mechanisms, and the role of potassium channels in cognitive function.

Research Applications
TREK-1 channel modulationneuroplasticity mechanismsneuroprotection studiespotassium channel biologysynaptic plasticity researchneurogenesis studiesneurotrophic signaling pathways
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution with bacteriostatic water, maintain at 2-8°C and use within 30 days. Standard peptide handling precautions apply.

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Melanocortin System Research

Melanocortin receptor pharmacology — MC3R, MC4R, and opioid receptor research tools.

Melanocortin Receptor Agonist≥98%

PT-141 (Bremelanotide)

Palatin Technologies research, United States
A cyclic heptapeptide melanocortin agonist with preferential activity at MC3R and MC4R—a Melanotan II metabolite engineered for selective melanocortin receptor research.

PT-141 emerged from structure-activity relationship studies of Melanotan II, a synthetic α-MSH analogue. While Melanotan II activates multiple melanocortin receptor subtypes (MC1R through MC5R), its metabolite PT-141 demonstrates preferential activity at MC3R and MC4R with reduced MC1R activation—eliminating much of the pigmentation effect while retaining central melanocortin activity. This selectivity makes PT-141 invaluable for dissecting the distinct roles of melanocortin receptor subtypes.

MC3R and MC4R, expressed primarily in the hypothalamus, regulate energy balance, autonomic function, and motivated behaviors through melanocortin signaling. PT-141 enables researchers to study these central melanocortin pathways without the confounding peripheral effects of broader melanocortin activation, making it the preferred tool for investigating hypothalamic melanocortin biology.

Research Applications
Melanocortin receptor subtype pharmacologyMC3R/MC4R signaling researchcentral melanocortin pathway studiesreceptor selectivity researchhypothalamic signaling mechanismsmelanocortin system biology
Molecular Profile
FormulaC50H68N14O10
CAS189691-06-3
MW1025.2 g/mol
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution with bacteriostatic water, maintain at 2-8°C and use within 30 days. The cyclic structure provides enhanced proteolytic stability.

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Opioid Peptide≥98%

Dermorphin (5mg)

Isolated from Phyllomedusa frogs, South America
A naturally occurring heptapeptide with extraordinary μ-opioid receptor selectivity—notable for its D-alanine residue and exceptional potency in opioid receptor research.

Dermorphin stands as one of pharmacology's most intriguing discoveries. Isolated from the skin secretions of South American Phyllomedusa frogs, this heptapeptide contains an unusual D-alanine in position 2—one of the rare instances of D-amino acids in biologically active peptides. This structural quirk contributes to dermorphin's exceptional properties: nanomolar μ-opioid receptor affinity, selectivity ratios exceeding 1000:1 for μ over δ and κ receptors, and resistance to peptidase degradation.

The peptide's extraordinary selectivity and potency have made it an essential tool in opioid receptor biology—enabling precise study of μ-opioid receptor pharmacology, structure-activity relationships, and receptor-ligand interactions. Researchers investigating opioid signaling mechanisms, studying receptor binding kinetics, or exploring the structural determinants of receptor selectivity consistently rely on dermorphin as a reference μ-selective agonist.

Research Applications
μ-opioid receptor pharmacologyreceptor subtype selectivity studiesopioid receptor binding kineticsstructure-activity relationshipsreceptor signaling mechanismsD-amino acid peptide biologyopioid tolerance mechanisms
Molecular Profile
FormulaC40H50N8O10
CAS77614-16-5
MW802.9 g/mol
Handling & Storage

Store lyophilized at -20°C protected from moisture and light. Upon reconstitution with sterile or bacteriostatic water, maintain at 2-8°C and use within 30 days. The D-amino acid provides proteolytic resistance.

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Cosmetic & Dermatological Research

Neurotoxins and dermatological research compounds for neuromuscular and skin biology.

Neurotoxin ProteinPharmaceutical grade

Botulinum Toxin Type A (100 Units)

Clostridium botulinum, pharmaceutical production
The most potent biological toxin known—a 150 kDa metalloprotease that cleaves SNAP-25 with absolute specificity, making it essential for studying synaptic vesicle fusion and neurotransmitter release.

Botulinum neurotoxin type A represents the gold standard for studying exocytosis. This large protein complex, produced by Clostridium botulinum, consists of a heavy chain (responsible for binding and internalization) and a light chain (the zinc-dependent endopeptidase that cleaves SNAP-25). By specifically cleaving SNAP-25—a protein essential for SNARE complex formation—BoNT/A prevents synaptic vesicles from fusing with the presynaptic membrane, completely blocking neurotransmitter release.

This exquisite molecular specificity makes botulinum toxin invaluable beyond its clinical applications. Researchers studying SNARE protein biology, investigating synaptic vesicle fusion mechanisms, exploring neuromuscular junction physiology, or dissecting the molecular machinery of exocytosis rely on BoNT/A's specific, irreversible SNAP-25 cleavage. The toxin serves as a molecular scalpel that precisely disrupts a single step in neurotransmitter release.

Research Applications
SNARE protein biologysynaptic vesicle fusion mechanismsneuromuscular junction researchacetylcholine release studiesexocytosis researchpresynaptic signalingmetalloprotease mechanism studies
Molecular Profile
CAS93384-43-1
MW~150 kDa (holotoxin)
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution, use immediately or store at 2-8°C for a maximum of 4 hours—this protein loses activity rapidly in solution. Handle with extreme care following institutional biosafety protocols.

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Neurotoxin ProteinPharmaceutical grade

Botulinum Toxin Type A (200 Units)

Clostridium botulinum, pharmaceutical production
The most potent biological toxin known—a 150 kDa metalloprotease that cleaves SNAP-25 with absolute specificity, making it essential for studying synaptic vesicle fusion and neurotransmitter release.

Botulinum neurotoxin type A represents the gold standard for studying exocytosis. This large protein complex, produced by Clostridium botulinum, consists of a heavy chain (responsible for binding and internalization) and a light chain (the zinc-dependent endopeptidase that cleaves SNAP-25). By specifically cleaving SNAP-25—a protein essential for SNARE complex formation—BoNT/A prevents synaptic vesicles from fusing with the presynaptic membrane, completely blocking neurotransmitter release.

This exquisite molecular specificity makes botulinum toxin invaluable beyond its clinical applications. Researchers studying SNARE protein biology, investigating synaptic vesicle fusion mechanisms, exploring neuromuscular junction physiology, or dissecting the molecular machinery of exocytosis rely on BoNT/A's specific, irreversible SNAP-25 cleavage. The toxin serves as a molecular scalpel that precisely disrupts a single step in neurotransmitter release.

Research Applications
SNARE protein biologysynaptic vesicle fusion mechanismsneuromuscular junction researchacetylcholine release studiesexocytosis researchpresynaptic signalingmetalloprotease mechanism studies
Molecular Profile
CAS93384-43-1
MW~150 kDa (holotoxin)
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution, use immediately or store at 2-8°C for a maximum of 4 hours—this protein loses activity rapidly in solution. Handle with extreme care following institutional biosafety protocols.

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Tissue Protection & Repair (Advanced)

Next-generation tissue protection — innate repair receptor agonists and targeted therapeutics.

Innate Repair Receptor Agonist≥98%

ARA-290 (10mg)

Derived from erythropoietin research, Netherlands
An 11-amino acid fragment of erythropoietin engineered to selectively activate the innate repair receptor—providing tissue protection and anti-inflammatory signaling without erythropoietic activity.

ARA-290 represents molecular refinement of erythropoietin's tissue-protective properties. While full-length EPO stimulates red blood cell production through the classical EPO receptor, it also activates a distinct receptor complex called the innate repair receptor (IRR or tissue-protective receptor)—a heteromeric complex that triggers cell protection, reduces inflammation, and promotes tissue repair. ARA-290, an 11-amino acid EPO-derived peptide, selectively activates the IRR without engaging the erythropoietic EPO receptor.

This separation of functions enables clean investigation of EPO's tissue-protective mechanisms without the confounding hematological effects. Research has demonstrated ARA-290's effects in neuropathy models, ischemia-reperfusion injury, and inflammatory conditions—all mediated through IRR signaling pathways distinct from classical EPO effects. The peptide provides a unique tool for studying tissue protection mechanisms and innate repair receptor biology.

Research Applications
Innate repair receptor signalingtissue protection mechanismsEPO receptor biologyneuroprotection studiesanti-inflammatory pathwaysischemia-reperfusion injury modelsdiabetic neuropathy research
Molecular Profile
FormulaC51H84N16O21
CAS1448671-31-5
MW1257.3 g/mol
Handling & Storage

Store lyophilized at -20°C. Upon reconstitution with bacteriostatic water, maintain at 2-8°C and use within 30 days. This peptide demonstrates good stability in solution.

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