Research Dossier on GHK-Cu / KPV / BPC-157 / TB500 (Blend)

Classification & Molecular Identity

Component overview

• GHK-Cu – a tripeptide–copper(II) complex (Gly-His-Lys·Cu²⁺). The free peptide GHK (M_r ≈ 340.4 g·mol⁻¹) forms a high-affinity complex with Cu²⁺; coordination involves the imidazole N of His and backbone nitrogens/oxygen donors, producing a redox-buffering Cu(II) environment. Endogenous GHK and GHK-Cu occur in human plasma, saliva, and urine. PubMed+1

• KPV – Lys-Pro-Val, the C-terminal tripeptide of α-MSH (melanocortin family). KPV displays anti-inflammatory activity in vitro and in vivo and can enter epithelial cells via the di/tri-peptide transporter PepT1. PMC

• BPC-157 – a 15-mer peptide described as the “Stable Gastric Pentadecapeptide,” frequently reported in preclinical models of tissue protection and repair across organ systems. Structure and sequences are published in the BPC literature; it is posited to be native to gastric juice, though human endogenous status is debated. Gut N Liver+1

• TB500 (“Tβ4-derived”) – in peer-reviewed science, effects ascribed to TB500 are typically investigated using thymosin β4 (Tβ4), a 43-aa actin-sequestering polypeptide, and/or its bioactive fragments (notably Ac-SDKP). In the academic literature, Tβ4 is linked to cell migration, angiogenesis, and tissue repair; TB500 itself is a market term, not a distinct sequence in primary literature. For scientific accuracy we reference Tβ4 and Tβ4-derived fragments. PubMed+2PubMed+2

Note on composite products. The scientific literature does not describe controlled trials of a four-component GHK-Cu/KPV/BPC-157/Tβ4 mixture. Evidence for each component exists separately (and sometimes for pairs), but blend-level pharmacodynamics, pharmacokinetics, and safety are Not established. This dossier synthesizes component-level evidence and explicitly flags knowledge gaps for the KLOWcombination.

Discovery history (lab, year, species)

• GHK (later GHK-Cu). Identified from human plasma; subsequently shown to stimulate collagen synthesis in fibroblasts at pico- to nanomolar concentrations (maximal around 10⁻⁹ M). PubMed

• KPV. Characterized as the C-terminal α-MSH tripeptide; topical and mucosal anti-inflammatory activity demonstrated in models of colitis and dermatitis; PepT1-mediated uptake corroborated. PMC

• BPC-157. Reported since the 1990s across rodent models of ulcer, tendon/ligament, and vascular injury; numerous dosing paradigms (ng–µg·kg⁻¹) have been published; modern reviews collate these findings. PubMed+1

• Tβ4 / fragments. Demonstrated to accelerate wound healing and promote angiogenesis in rodent skin, cardiac, and CNS-injury models; Ac-SDKP, a tetrapeptide fragment, is widely studied for anti-fibrotic actions. PubMed+2PubMed+2

Endogenous vs synthetic origin

• GHK-Cu – endogenous peptide–metal complex; research materials are synthetic/recombinant. PMC

• KPV – endogenous tripeptide sequence (from α-MSH); research supply is synthetic. PMC

• BPC-157 – often described as native to gastric juice; definitive endogenous status in humans remains debated; research materials are synthetic. PMC

• Tβ4/Ac-SDKP – endogenous (Tβ4 abundant in many tissues; Ac-SDKP generated from Tβ4 and degraded by ACE); research supply is recombinant/synthetic. PMC

Homologs, analogs, derivatives

• GHK-Cu: related Cu(II)-binding tripeptides include AHK-Cu; albumin DAHK–Cu (ATCUN motif) is the dominant plasma Cu(II) binder that competes with lower-abundance peptide ligands in vivo. PMC

• KPV: melanocortin analogs (e.g., KdPT) retain anti-inflammatory activity without pigment induction. PubMed

• BPC-157: classed with cytoprotective gastric peptides; literature reports multiple ng–µg·kg⁻¹ dose-effects across systems. Frontiers

• Tβ4 fragments: Ac-SDKP (N-acetyl-Ser-Asp-Lys-Pro) exhibits anti-fibrotic activity in heart/kidney/lung injury models. Europe PMC

Historical Development & Research Trajectory

Key milestones

• GHK-Cu (1970s–2000s): Discovery in human plasma → fibroblast and dermal models showing collagen and proteoglycan upregulation and modulation of MMP/TIMP balance; later gene-program analyses proposed broader protective signatures. PubMed+1

• KPV (1998–2010s): Proof of anti-inflammatory efficacy in keratinocytes and murine colitis; PepT1 dependencedemonstrated (KPV ineffective in PepT1-knockout mice), anchoring intestinal uptake/bioactivity mechanisms. PMC+1

• BPC-157 (1999–2025): Extensive rodent literature across GI, vascular, tendon, CNS and multi-organ injury with reproducible ng–µg·kg⁻¹ effects; 2011–2025 reviews summarize pleiotropy; human clinical datasets remain limited. Gut N Liver+1

• Tβ4 / Ac-SDKP (1999–2024): Wound-healing acceleration, angiogenesis and cell migration in skin and cornea; cardiac/renal anti-fibrosis via Ac-SDKP; recent reports continue in surgical flap and ischemia models. PubMed+2PubMed+2

Paradigm shifts & controversies

1. From single-pathway to multi-modal repair:
   GHK-Cu moved from a “dermal collagen” factor to a metal-homeostasis/redox buffering and gene-reprogramming modulator; KPV from melanocortin mimicry to PepT1-targeted anti-inflammation; Tβ4 from “actin-binding” to angiogenesis/fibrosis axes; BPC-157 from GI cytoprotection to system-wide models. Translation to large, modern RCTs is limited for all four. PMC+3PMC+3PMC+3

2. Composite use (KLOW):
   Despite frequent co-marketing, no peer-reviewed, controlled studies test the exact four-component KLOW mixture. Synergy/antagonism and net safety at blend-level are Not established.

3. Terminology realism:
   “TB500” is a market term; academic evidence is for Tβ4 and its fragments. Extrapolating TB500 claims requires caution. PubMed

Evolution of interest

• GHK-Cu: from dermatology to metal biology and systems genomics;

• KPV: from melanocortin pharmacology to intestinal barrier / PepT1 targeting;

• BPC-157: broadening to vascular and CNS models;

• Tβ4/Ac-SDKP: expanding anti-fibrosis and cardiac/renal repair interest. PMC+1

Mechanisms of Action

Primary and secondary interactions (component-level)

• GHK-Cu
  High-affinity Cu(II) chelation forms a relatively redox-inert complex that buffers copper-driven ROS chemistry; promotes ECM remodeling (collagen I/III, decorin), and modulates MMP-2/TIMPs in fibroblasts. Albumin (DAHK–Cu) is the dominant extracellular Cu(II) binder in plasma; GHK-Cu likely functions as a minor, exchangeable pool influencing local signaling and cellular Cu uptake. PubMed+1

• KPV
  Exhibits anti-inflammatory actions in epithelial/immune models, reducing NF-κB-linked cytokines; PepT1facilitates uptake in inflamed colon where PepT1 is induced. Some data suggest MC1R-independent anti-inflammation despite its α-MSH origin, indicating distinct downstream effectors. PMC+1

• BPC-157
  Reported cytoprotective effects across GI, vascular, ligament/tendon and CNS injury models. Proposed mechanisms include angiogenesis modulation, interaction with NO pathways, and support of granulation/tendon matrix organization; mechanistic consensus remains incomplete and often model-specific. Frontiers

• Tβ4 / Ac-SDKP
  Tβ4 binds G-actin, supporting cell migration, angiogenesis, and re-epithelialization; Ac-SDKP shows anti-fibrotic actions via ACE-dependent turnover and downstream suppression of myofibroblastactivation/inflammation. PubMed+1

Blend-level inference: Mechanistic complementarity is plausible (ECM/angiogenesis (GHK-Cu, Tβ4) + anti-inflammation (KPV) + cytoprotection (BPC-157)), but pharmacodynamic interaction data for the four-way combination are Not established.

Intracellular signaling pathways (selected)

• GHK-Cu: ECM gene programs (collagens/decorin), MMP-2/TIMP modulation; redox-responsive pathways via copper buffering; multiple transcriptional changes reported in omics screens. PMC

• KPV: suppression of NF-κB targets and inflammatory mediators in intestinal/keratinocyte models; PepT1-dependent epithelial entry; activity partly independent of MC1R. PMC+1

• BPC-157: proposed ties to NO-system balance and angiogenic signaling in preclinical models (varies by tissue). Frontiers

• Tβ4/Ac-SDKP: cytoskeletal regulation (actin), integrin-linked signaling, pro-angiogenic cascades; Ac-SDKP intersects fibrosis pathways (e.g., TGF-β/Smad context). Frontiers+1

CNS vs peripheral effects

• Peripheral evidence is strongest for all four (dermis, GI mucosa, vascular, tendon/ligament, cardiac/renal). Direct CNS penetration is uncertain for the larger components (Tβ4; KP-54 vs KP-10 analogy)—Not established for blend-level CNS actions.

Hormonal, metabolic, immune interactions

• KPV influences mucosal immunity and barrier function in colitis models;

• GHK-Cu down-tunes inflammatory markers while remodeling ECM;

• BPC-157 reports multi-organ anti-inflammatory and vascular effects;

• Tβ4/Ac-SDKP reduce fibrotic remodeling in heart/kidney/lung models. PMC+3PMC+3PMC+3

Evidence grading (A–C)

• A (replicated preclinical domains):
  GHK-Cu stimulation of collagen and matrix remodeling; KPV anti-inflammation via PepT1; Tβ4-promoted angiogenesis/wound-healing; Ac-SDKP anti-fibrosis; BPC-157 GI/soft-tissue protection across multiple rodent labs. Frontiers+4PubMed+4PMC+4

• B (translational/limited human):
  Cosmetic-grade dermal studies with GHK-Cu; small/focused surgical and ocular applications for Tβ4 (varied); BPC-157 human-grade evidence is limited; KPV human data focus on mechanism and delivery, not large clinical outcomes. PMC

• C (blend-level / chronic therapy):
  No controlled, peer-reviewed studies for the four-component KLOW blend; long-term safety/PK of co-administration Unknown.

Pharmacokinetics & Stability

Absorption, distribution, metabolism, excretion (ADME)

• GHK-Cu
  Human PK is Not established. In plasma, albumin (DAHK)–Cu dominates Cu(II) binding; GHK-Cu likely acts as a minor exchangeable pool with local effects; systemic distribution and clearance kinetics remain unclear. PMC

• KPV
  PepT1 mediates epithelial uptake; PepT1 is induced in inflamed colon (IBD), enabling oral/rectal epithelial entry in models. Systemic PK parameters are limited; nano-delivery can reduce effective dose ~10³–10⁴-fold in preclinical colitis paradigms. PMC+1

• BPC-157
  Human PK is Not established. Rodent studies report activity with oral (in water) and parenteral routes at 10 ng–10 µg·kg⁻¹ ranges (model-dependent). Frontiers

• Tβ4 / Ac-SDKP
  Tβ4 (43 aa) is expected to have limited V_d and rapid proteolysis; Ac-SDKP is ACE-metabolized. Quantitative human PK in standardized form is limited; local/topical delivery is common in animal models. PMC

Plasma half-life & degradation

• GHK-Cu: Not established in humans; in vitro complex is stable under neutral pH; in vivo exchange with albumin/glutathione is expected. PMC

• KPV: Short, tripeptide; PepT1-facilitated uptake and intracellular signaling may outlast plasma exposure; hepatorenal peptidases degrade systemically. PMC

• BPC-157: Not well-defined; bioactivity observed despite presumed rapid peptidase degradation in plasma. Not established with validated human assays. Frontiers

• Tβ4/Ac-SDKP: Tβ4 rapidly cleared as a polypeptide; Ac-SDKP turnover via ACE; half-life values vary by species and assay. PMC

Stability (in vitro & in vivo); storage/reconstitution

• Assay-dependent stability is reported for all four; standardized, product-agnostic shelf-life and reconstitutioncurves for research vials are Not established in peer-reviewed sources. Standard peptide handling (low temperature, protect from light, avoid repeated freeze–thaw) applies.

Preclinical Evidence

GHK-Cu (selected)

• Dermal fibroblasts – collagen synthesis stimulated starting 10⁻¹²–10⁻¹¹ M, maximal near 10⁻⁹ M (investigational concentrations used in study Maquart 1988). PubMed

• Tissue remodeling – reviews aggregate increases in decorin, glycosaminoglycans, balanced MMP-2/TIMPregulation, and anti-oxidative effects via copper redox buffering. PMC

KPV (selected)

• Colitis models – anti-inflammatory effects in two murine colitis models; MC1R-independent features noted (investigational doses in murine colitis used in study Kannengiesser 2008). PubMed

• PepT1 dependence – KPV prevents colitis-associated carcinogenesis in WT but not PepT1-KO mice, confirming transporter-mediated uptake (investigational regimens in Viennois 2016). PMC

• Nanodelivery – KPV-loaded nanoparticles achieve ~12,000-fold dose reduction vs free KPV with comparable efficacy in preclinical colitis (investigational nanodose used in Laroui 2010). Gastro Journal

BPC-157 (selected)

• Tendon/ligament/vascular models – multiple rodent studies show faster healing of tendons and anastomoses; typical investigational doses include 10 µg·kg⁻¹, 10 ng·kg⁻¹, 10 pg·kg⁻¹, given i.p. or p.o. (e.g., Staresinic 2003; Jelovac 1999; Seiwerth 2021). PubMed+2ScienceDirect+2

• GI cytoprotection – evidence for protection/repair in ulcer and fistula models; e.g., oral water (10 µg·kg⁻¹) vs i.p.(10 µg·kg⁻¹/10 ng·kg⁻¹) paradigms (investigational regimens). Frontiers

Tβ4 / Ac-SDKP (selected)

• Skin wound healing – topical or parenteral Tβ4 accelerates re-epithelialization and angiogenesis; doses include 2.5–5 µg per 50 µL topical or 6 mg·kg⁻¹ i.p. in rodent models (investigational doses in Malinda 1999; Philp 2004; Xiong 2010). ScienceDirect+2PubMed+2

• Anti-fibrosis (Ac-SDKP) – reduces cardiac/renal fibrosis in hypertensive and post-injury models; ACE as a key turnover enzyme and pharmacologic node. Europe PMC

Comparative efficacy/safety (preclinical)

• Efficacy – each component shows benefit vs vehicle in its domain (ECM remodeling, anti-inflammation, cytoprotection, angiogenesis/anti-fibrosis).

• Safety – no GLP-grade, long-term toxicology packages for all four combined; component-level toxicology is heterogeneous and often model-limited.

• Limitations – inter-species differences, variable endpoints, and reliance on small cohorts are common; blend-leveleffects are unknown.

Human Clinical Evidence

Important: No controlled human trials evaluate the four-component KLOW blend. Component-level human evidence remains domain-specific and limited in scale.

GHK-Cu

• Dermal/appearance outcomes – cosmetic-grade studies report improvements in skin density, firmness, appearance over 8–12 weeks; controlled comparisons vs vitamin C/retinoic acid exist but are not drug-approval studies; standardized histologic endpoints vary. (Investigational topical courses summarized in Pickart & Margolina 2018 review.) PMC

KPV

• Direct clinical trials of KPV as a single agent are limited; translational focus is on PepT1-targeted delivery strategies and preclinical mucosal models, with a view to colitis/dermatology. Robust Phase II/III data are not available. Frontiers

BPC-157

• Human datasets are limited and heterogeneous (case-series, small trials); most evidence remains preclinical. Review articles frequently cite Curr Pharm Des 2011 and updates (2020–2025) synthesizing rodent findings across systems; registered, indication-specific late-phase trials are sparse. Gut N Liver+1

Tβ4 / fragments

• Ocular/dermal pilot studies and clinical explorations have been reported in the broader Tβ4 literature; multi-center, indication-specific Phase III data are limited. Reviews outline wound repair and ischemia contexts. Frontiers

Safety signals/adverse events (human)

• Component-level short-term use (e.g., topical GHK-Cu) generally shows acceptable local tolerability; systemic safety for BPC-157 and Tβ4 derivatives in large, controlled human programs remains Not established. Combination safety for KLOW is Unknown. PMC

ClinicalTrials.gov IDs

• No trial IDs found for the four-way combination. Component-level searches yield small/early programs or cosmetic contexts; comprehensive therapeutic RCTs are limited.

Comparative Context

Related peptides by function

• ECM/angiogenesis – GHK-Cu, Tβ4

• Anti-inflammation / mucosal barrier – KPV, BPC-157

• Anti-fibrosis – Ac-SDKP (Tβ4 fragment)

Advantages (research perspective)

• Mechanistic complementarity across ECM remodeling, angiogenesis, anti-inflammation, and cytoprotection.

• Distinct entry points—metal buffering (GHK-Cu), transporter-enabled epithelial uptake (KPV/PepT1), cytoprotective peptide biology (BPC-157), actin/angiogenesis/fibrosis axes (Tβ4/Ac-SDKP). PMC+3PMC+3PMC+3

Disadvantages / constraints

• Blend-level data lacking (PK, PD, safety, dose optimization).

• Potential competition/interference (e.g., copper binding equilibria with albumin vs GHK, or overlapping angiogenic signaling) is unquantified.

• Regulatory-grade clinical evidence is limited for each component in therapeutic settings.

Research category placement

• Preclinical composite of four research peptides targeting tissue repair biologies; appropriate as a hypothesis-generating framework only until blend-level data exist.

Research Highlights

• GHK-Cu boosts collagen in fibroblasts at pM–nM with supportive human dermal observations (cosmetic-grade). PubMed+1

• KPV leverages PepT1—a transporter up-regulated in inflamed colon—to achieve anti-inflammation; PepT1-dependence confirmed in knockout models. PMC+1

• BPC-157 repeatedly improves healing in rodent tendon/vascular/intestinal models at 10 pg–10 µg·kg⁻¹ ranges. PubMed+1

• Tβ4/Ac-SDKP deliver angiogenesis and anti-fibrosis signals across skin, heart, and kidney models. PubMed+1

Conflicting/uncertain areas

• Blend-level efficacy/safety – Not established; no pharmacologic interaction studies.

• Human PK/PD for BPC-157 and Tβ4 derivatives – limited; standardized assays lacking. PMC

• Long-term risk (e.g., unregulated angiogenesis or fibrotic remodeling) – Unknown in composite use.

Potential Research Applications (no clinical claims; research-use framing)

1. Orthogonal mechanistic mapping

   • Use GHK-Cu (ECM/redox), KPV (PepT1-mediated anti-inflammation), BPC-157(cytoprotection/angiogenesis), Tβ4/Ac-SDKP (angiogenesis/anti-fibrosis) individually and in pairwisecombinations to quantify additivity/synergy, using standardized wound-healing and colitis models (histology, RNA-seq, proteomics). PMC+3PMC+3PMC+3

2. Transport & delivery optimization

   • Exploit PepT1 induction in inflamed mucosa for KPV or co-cargo delivery (e.g., nanoparticles) and assess whether co-delivery with BPC-157 or GHK-Cu modifies barrier integrity and angiogenic markers. Gastro Journal

3. Angio-fibrosis balance assays

   • Parallel assays of angiogenesis (tube formation, perfused microvessels) and fibrosis (myofibroblast markers, collagen cross-linking) to map Tβ4/Ac-SDKP with/without GHK-Cu; evaluate risk of unwanted neovascularization. PubMed+1

4. PK-aware study design

   • Measure tissue levels (LC-MS/ICP-MS for copper species) and functional copper speciation alongside peptide levels to understand GHK-Cu/albumin/glutathione exchange; define exposure windows for pairwise combinations before attempting a four-component blend. PMC

5. Safety characterization

   • GLP-style repeat-dose studies for the blend: clinical chemistry, histopathology, angiogenesis-related and fibrosis panels, and immunogenicity; screen for drug–drug and metalloprotein interactions.

Safety & Toxicology

Preclinical toxicity (component-level)

• GHK-Cu – topical dermal use appears well-tolerated in small studies; systemic safety at pharmacologic exposures is Not established. PMC

• KPV – favorable rodent tolerability in colitis/dermatitis models; clinical-grade chronic safety is Not established. PMC

• BPC-157 – extensive rodent literature notes benefit at ng–µg·kg⁻¹ without major toxicity signals in model timeframes; GLP-conformant tox packages are limited. Frontiers

• Tβ4/Ac-SDKP – generally well-tolerated in preclinical studies; long-term systemic safety across species and doses varies and remains under characterization. Frontiers

Known/theoretical molecular risks

• Unintended angiogenesis or fibrotic remodeling with angiogenic/ECM-active agents (GHK-Cu, Tβ4) in susceptible tissues – Unknown at blend-level. PubMed

• Copper handling – systemic Cu(II) redistribution by GHK-Cu is modulated by dominant albumin (DAHK)–Cuand intracellular ligands; off-target copper effects at therapeutic levels are not quantified. PMC

• Immunogenicity – small peptides typically low risk, larger Tβ4 higher theoretical risk; blend-level immunogenicity is Unknown.

Human safety observations

• Where reported (e.g., topical GHK-Cu), short-term tolerability is acceptable; systemic/adjuvant safety for BPC-157 and Tβ4-derivatives remains Not established in large RCTs. Combination (KLOW) safety: Unknown. PMC

Limitations & Controversies

• No blend-level trials. There are no peer-reviewed, controlled studies evaluating GHK-Cu/KPV/BPC-157/Tβ4together.

• Heterogeneous evidence quality. Some domains rely on older animal studies, small cohorts, or cosmetic-gradeendpoints.

• Terminology. “TB500” lacks a unique peer-reviewed sequence; academic evidence addresses Tβ4/Ac-SDKP. PubMed

• PK gaps. Human PK for BPC-157 and Tβ4 is limited; copper speciation in vivo with GHK-Cu remains incompletely quantified. PMC

Future Directions

1. Pairwise interaction studies (GHK-Cu+Tβ4; KPV+BPC-157; etc.) with defined PK/PD and angiogenesis–fibrosis balance endpoints prior to any four-component effort.

2. Mechanistic deconvolution using single-cell RNA-seq and spatial proteomics in wound/colitis models to identify cell-type-specific responses and off-target risks.

3. Copper metallomics to map GHK-Cu exchange with albumin/glutathione and quantify intracellular Cu(II/I)pools during ECM remodeling. PMC

4. PepT1-targeted delivery strategies for KPV (and possibly co-cargo) to reduce systemic exposure while maximizing mucosal effects; expand to human translational studies if justified. Gastro Journal

5. GLP safety & chronic dosing in relevant species for the blend, including immunogenicity, organ histopathology, and oncology-adjacent surveillance (angiogenesis).

References

1. Maquart FX, et al. Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex GHK-Cu. FEBS Lett. 1988. PMID: 3169264. PubMed

2. Pickart L, Margolina A. Regenerative and Protective Actions of the GHK-Cu Peptide. Int J Mol Sci. 2018. PMCID: PMC6073405. PMC

3. Dalmasso G, et al. PepT1-mediated KPV uptake reduces intestinal inflammation. Gastroenterology. 2008; mechanistic PMC report. PMCID: PMC2431115. PMC

4. Viennois E, et al. Critical role of PepT1 in colitis-associated carcinogenesis; KPV prevention depends on PepT1. Oncotarget. 2016. PMCID: PMC4957955. PMC

5. Kannengiesser K, et al. KPV anti-inflammation partly independent of MC1R signaling in murine colitis.Inflamm Bowel Dis. 2008. PMID: 18092346. PubMed

6. Laroui H, et al. Nanoparticle delivery enables ~12,000-fold KPV dose reduction in colitis model.Gastroenterology (Imaging & Adv Tech). 2010. (PDF). Gastro Journal

7. Sikiric P, et al. Stable Gastric Pentadecapeptide BPC-157: GI tract therapy (2011) & updates (2020–2025 reviews). Curr Pharm Des. 2011; Gut Liver. 2020; Pharmaceutics. 2023; Biomedicines/MDPI. 2024. PMIDs/PMC: 21406437 (review cited), PMC11053547, 627533. Gut N Liver+2PMC+2

8. Staresinic M, et al. BPC-157 accelerates healing (anastomosis/ligament models); 10 µg·kg⁻¹/10 ng·kg⁻¹/10 pg·kg⁻¹ i.p. J Physiol Paris. 2003. PMID: 14554208. PubMed

9. Jelovac N, et al. BPC-157 anti-ulcer/catalepsy models at 10 µg–100 pg·kg⁻¹. Eur J Pharmacol. 1999. (Abstract). ScienceDirect

10. Malinda KM, et al. Thymosin β4 accelerates wound healing. J Invest Dermatol. 1999. PMID: 10469335. PubMed

11. Philp D, et al. Tβ4 promotes angiogenesis and dermal repair in aged rodents. Ann N Y Acad Sci. 2004. PMID: 15037013. PubMed

12. Xiong Y, et al. Tβ4 improves outcomes in rat TBI at 6 mg·kg⁻¹ i.p. J Neurosurg. 2010. PMCID: PMC2962722. PMC

13. Cavasin MA, et al. Therapeutic potential of Tβ4 and derivative Ac-SDKP in cardiovascular disease.Cardiovasc Drug Rev. 2006. PMID: 17083265. Europe PMC

14. Wang W, et al. Tβ4–POP–Ac-SDKP axis in organ fibrosis (review). Int J Mol Sci. 2022. PMCID: PMC9655242. PMC

15. Dinparastisaleh R, et al. Antifibrotic/anti-inflammatory actions of α-MSH–derived peptides. Int J Mol Sci.2021. PMCID: PMC7827684. PMC

16. Xing Y, et al. Progress on the function and application of Tβ4 (overview). Front Endocrinol. 2021. PMCID: PMC8724243. PMC

17. Additional GHK-Cu technical context (albumin ATCUN competition, dermal outcomes) summarized in Pickart & Margolina 2018. PMC

Investigational doses highlighted above are study-specific and model-dependent; they do not constitute recommendations.

⚠️ Disclaimer This peptide (and any composite of these peptides) is intended strictly for laboratory research use. It is not FDA-approved or authorized for human use, consumption, or therapeutic application