Introduction: Two Peptides, Two Distinct Regenerative Research Pathways
Among the peptides most frequently discussed in tissue-repair and regenerative biology research, BPC-157 and TB-500 occupy a unique comparative position. Both are studied extensively in preclinical models for their roles in wound healing, angiogenesis, and musculoskeletal tissue repair – yet they arise from entirely different biological origins, act through distinct molecular mechanisms, and have accumulated markedly different depths of published evidence. Understanding these differences is essential for researchers designing comparative experiments, reviewing existing literature, or evaluating which compound is appropriate for a given research question.
BPC-157 is a synthetic pentadecapeptide (15 amino acids: GEPPPGKPADDAGLV) derived from a partial sequence of human gastric juice protein, first isolated and characterized by researchers at the University of Zagreb School of Medicine, led largely by the laboratory of Predrag Sikiric. Over 100 published preclinical studies have examined BPC-157 in gastrointestinal protection, tendon and ligament repair, muscle injury models, and vascular biology (Sikiric et al., PMC12195719; Chang et al., PMID 23782145).
TB-500 is a synthetic peptide corresponding to the biologically active region of Thymosin Beta-4 (Tβ4), a naturally occurring 43-amino-acid intracellular protein and the most abundant actin-monomer-binding (G-actin-sequestering) protein in mammalian cells. TB-4 research has an even longer publication history, dating to foundational work in the late 1990s (Malinda et al., PMID 10469335), and includes translational work that has progressed into Phase 3 human clinical trials for corneal and dermal applications under the designation RGN-259 (Sosne et al., PMID 30063853) – though it is important to note that TB-500 itself, as a shorter synthetic fragment sold for research purposes, has a comparatively narrower direct evidence base than its parent molecule Tβ4.
This article provides a structured comparative review of the mechanism of action, cellular and molecular effects, preclinical application domains, and research trajectories for both compounds, drawing exclusively on peer-reviewed, PubMed-indexed literature. The goal is to give peptide researchers a clear side-by-side reference for study design and literature review – not to make any claims about human therapeutic use.
Origin and Structural Background
BPC-157: Gastric Cytoprotective Origin
BPC-157 (also referenced in the literature as BPC 15, PL-10, PL 14736, and bepecin) is derived from a fragment of a larger gastric juice protein identified as having tissue-protective properties. Its parent designation, “Body Protection Compound,” reflects its initial characterization as a cytoprotective agent in the gastrointestinal mucosa. Critically, published pharmacokinetic research demonstrates that BPC-157 is unusually stable in gastric acid – a property almost no other peptide shares – giving it meaningful chemical stability in oral administration research models even though its systemic half-life after absorption remains short (Sikiric et al., PMC12195719).
Structurally, BPC-157 is a linear pentadecapeptide with the sequence Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val. Unlike growth-factor peptides that act through classical single-receptor binding, BPC-157’s mechanism appears to be pleiotropic – modulating multiple parallel systems (angiogenic, nitrergic, and growth factor receptor pathways) rather than acting as a ligand for one dedicated receptor (Seiwerth et al., PMID 41155565).
TB-500 / Thymosin Beta-4: Actin-Regulatory Origin
Thymosin Beta-4 belongs to the beta-thymosin family of highly conserved intracellular peptides. Its principal established biochemical function is G-actin sequestration: Tβ4 binds monomeric actin in a 1:1 ratio, regulating the pool of unpolymerized actin available for filament (F-actin) assembly. This actin-regulatory function underlies Tβ4’s role in cell motility, since cytoskeletal remodeling is a prerequisite for the migration of endothelial cells, fibroblasts, and keratinocytes into wound beds (Goldstein et al., PMID 17083265; Bock-Marquette et al., PMID 15565145).
TB-500, as sold for research purposes, is a synthetic peptide intended to reproduce the active region of the parent Tβ4 molecule, most often referencing the LKKTETQ actin-binding motif and associated active-region sequence. Researchers should note an important literature caveat: the overwhelming majority of PubMed-indexed studies were conducted using full-length Thymosin Beta-4, not the shorter synthetic “TB-500” fragment specifically. A 2024 scoping review found that “direct TB-500 evidence was limited to a single included study,” with the bulk of applicable mechanistic and efficacy data coming from full Tβ4 research (MDPI Applied Sciences scoping review, 2024). This distinction matters significantly for experimental design and literature citation practices.
Mechanism of Action: Comparative Analysis
BPC-157 Mechanistic Pathways
Preclinical research on BPC-157 has converged on several interlocking mechanistic themes:
1. VEGFR2-Mediated Angiogenesis. A pivotal study by Hsieh and colleagues demonstrated that BPC-157 promotes angiogenesis through increased expression and internalization of vascular endothelial growth factor receptor 2 (VEGFR2), activating the downstream VEGFR2-Akt-eNOS signaling cascade in a rat hind-limb ischemia model. Notably, this study found BPC-157 upregulated VEGFR2 expression without a corresponding increase in VEGF ligand itself – suggesting a VEGF-independent or VEGF-sensitizing angiogenic mechanism distinct from canonical growth-factor-driven angiogenesis (Hsieh et al., PMID 27847966).
2. Nitric Oxide (NO) System Modulation. BPC-157 has been shown across multiple studies to interact with both eNOS and iNOS pathways, promoting NO-dependent vascular relaxation and modulating the balance between protective and cytotoxic NO signaling. This dual role – supporting NO’s protective vasodilatory functions while apparently counteracting its cytotoxic and pro-inflammatory actions in ulcer and injury models – is described extensively in reviews by the Zagreb research group (Seiwerth et al., PMID 41155565; Sikiric et al., PMID 23782145).
3. FAK-Paxillin Pathway and Fibroblast Migration. In tendon fibroblast explant models, BPC-157 significantly accelerated tendon fibroblast outgrowth, survival under stress conditions, and in vitro migration. Mechanistic work localized this effect to activation of the focal adhesion kinase (FAK)-paxillin signaling pathway, a cascade central to cell-matrix adhesion and directional cell migration (Chang et al., PMID 21030672).
4. Growth Hormone Receptor Upregulation. A cDNA microarray screen of BPC-157-treated tendon fibroblasts identified growth hormone receptor (GHR) as one of the most significantly upregulated genes. Follow-up work confirmed that BPC-157 dose- and time-dependently increases GHR expression at both the mRNA and protein level, potentiating the proliferative effect of growth hormone on tendon fibroblasts – a distinct, receptor-crosstalk-based mechanism separate from direct angiogenic signaling (Chang et al., PMC6271067).
TB-500 / Thymosin Beta-4 Mechanistic Pathways
1. G-Actin Sequestration and Cell Migration. The foundational mechanism of Tβ4 is its binding of monomeric G-actin, which regulates the dynamic equilibrium between free actin monomers and polymerized actin filaments. Because directed cell migration requires continuous cytoskeletal remodeling, Tβ4’s actin-binding activity directly modulates the migratory capacity of endothelial cells, keratinocytes, and fibroblasts recruited to a wound site (Goldstein et al., PMID 17083265).
2. Integrin-Linked Kinase (ILK) Activation in Cardiac Tissue. Bock-Marquette and colleagues demonstrated that Tβ4 activates integrin-linked kinase (ILK) and promotes cardiomyocyte migration and survival following myocardial injury in mouse models – a mechanism proposed as a potential therapeutic target for cardiac repair research, distinct from BPC-157’s angiogenic pathway (Bock-Marquette et al., PMID 15565145).
3. Endothelial Progenitor Cell (EPC) Support and Angiogenesis. Tβ4 has been shown to promote survival and angiogenic function of endothelial progenitor cells, with Tβ4-treated EPCs improving cardiac function and enhancing repair of infarcted myocardium following transplantation in rodent ischemia models – indicating an angiogenic mechanism operating through progenitor cell biology rather than direct endothelial receptor modulation (Quan et al., PMID 28440414; Chiu et al., PMID 22817626).
4. Anti-Inflammatory and Anti-Apoptotic Signaling. Structure-function research localized specific Tβ4 sub-sequences to specific biological functions: the first four amino acids are associated with anti-inflammatory and antifibrotic effects, while amino acids 1–15 are linked to anti-apoptotic, cytoprotective activity – a modular functional architecture not reported for BPC-157 (Xu et al., PMC8724243).
Comparative Table: Mechanism Summary
To summarize the divergent mechanistic profiles for research design purposes:
- Primary molecular target: BPC-157 – multi-pathway/pleiotropic (VEGFR2, NOS, FAK, GHR); TB-500/Tβ4 – G-actin sequestration and ILK activation
- Core angiogenic mechanism: BPC-157 – VEGFR2 receptor upregulation/internalization; TB-500/Tβ4 – endothelial progenitor cell survival and migration support
- Primary cytoskeletal role: BPC-157 – indirect (via FAK-paxillin adhesion signaling); TB-500/Tβ4 – direct (actin monomer binding)
- Depth of direct compound-specific evidence: BPC-157 – over 100 studies using the specific 15-mer sequence; TB-500 – comparatively sparse, with most mechanistic data derived from full-length Tβ4 rather than the synthetic fragment itself
- Oral/gastric stability: BPC-157 – notably stable in gastric acid, a distinguishing pharmacokinetic property; Tβ4/TB-500 – not established as gastric-stable in the literature
Cellular Effects: Preclinical Findings in Detail
BPC-157: Gastrointestinal Protection
The original and most extensively replicated application domain for BPC-157 is gastrointestinal mucosal protection. In a rat model of acute and chronic gastric ulcer, both intramuscular and intragastric administration of BPC-157 significantly reduced ulcer area and accelerated healing, with inhibition ratios of ulcer formation ranging from 45.7% to 65.6% relative to saline controls, and intramuscular administration outperforming intragastric administration (Xiao et al., PMID 15052688). This gastroprotective effect has since been extended to models of clopidogrel-induced gastric injury, where BPC-157 co-treatment significantly reduced ulcer recurrence rate and ulcer index scores (PMC7763470).
BPC-157: Musculoskeletal Tissue Repair
BPC-157’s most cited research domain beyond the GI tract is musculoskeletal soft tissue repair. In a rat Achilles tendon transection model, BPC-157 administration produced improvements across biomechanical measures (increased load of failure, Young’s modulus of elasticity), functional measures (higher Achilles Functional Index values), and histological measures (superior fibroblast, reticulin, and collagen formation) compared to controls (Krivic et al., PMID 14554208). Parallel work on medial collateral ligament (MCL) transection found BPC-157 improved ligament healing when administered either systemically (intraperitoneally at 10 µg or 10 ng/kg) or locally as a topical cream preparation (Krivic et al., PMID 20225319). In tendon-to-bone healing models following Achilles detachment, BPC-157 promoted healing that otherwise did not occur spontaneously, improving functional, biomechanical, and histological outcomes across a 21-day observation window (Klicek et al., PMID 16583442).
In skeletal muscle injury models, BPC-157 improved healing following muscle crush injury in rats and counteracted the impairment of healing caused by corticosteroid co-administration – an important finding given that corticosteroids are known to impair tissue repair in many contexts (Pevec et al., PMID 20190676; Mihaljevic et al., PMID 18668315).
TB-500/Tβ4: Dermal Wound Healing
The foundational 1999 study by Malinda and colleagues, published in the Journal of Investigative Dermatology, established that Tβ4 enhanced wound healing in a rat full-thickness wound model, with keratinocyte migration stimulated 2-3-fold over baseline when as little as 10 picograms of Tβ4 was introduced to the assay – indicating extraordinarily high biological potency at minute concentrations (Malinda et al., PMID 10469335).
TB-500/Tβ4: Corneal and Ocular Repair
Tβ4’s most clinically advanced research domain is ophthalmic. Sosne and colleagues demonstrated that Tβ4 promotes corneal wound healing and decreases inflammation in vivo following alkali injury, with subsequent work characterizing Tβ4 as a “novel corneal wound healing and anti-inflammatory agent” mediating cell migration through hemidesmosome and desmosome-associated adhesion pathways (Sosne et al., PMID 11950239; Sosne et al., PMC2701135). This ocular research program progressed to human Phase 3 clinical trials for dry eye syndrome and neurotrophic keratopathy under the compound designation RGN-259 – representing one of the furthest clinical translations of any peptide discussed in the CRP research library, though again, this trial used full-length Tβ4-derived formulations, not the shorter synthetic TB-500 fragment (Sosne et al., PMID 30063853; Sosne et al., PMID 23050816).
TB-500/Tβ4: Cardiac Repair
In myocardial infarction models, Tβ4 facilitated cardiac repair by promoting cardiomyocyte migration and survival through ILK pathway activation (Bock-Marquette et al., PMID 15565145). Later work demonstrated that Tβ4-treated endothelial progenitor cells improved cardiac function and enhanced repair of infarcted myocardium following transplantation, and that controlled local release of Tβ4 from injected collagen matrices within the infarct zone enhanced angiogenesis and cardiomyocyte presence necessary for structural repair (Quan et al., PMID 28440414; Chiu et al., PMID 22817626; Cavasin et al., PMID 17083265).
Applications in Ongoing Research
Researchers actively studying these two compounds should note their differing “centers of gravity” within the regenerative biology literature:
BPC-157 research clusters most heavily around: (1) gastrointestinal mucosal protection and ulcer healing, (2) tendon, ligament, and muscle repair following transection or crush injury, (3) angiogenesis and vascular repair in ischemia models, and (4) emerging work on neuroprotection in Parkinson’s and Alzheimer’s disease animal models, and anti-tumor activity in vivo and in vitro (Sikiric et al., PMC12195719).
TB-500/Tβ4 research clusters most heavily around: (1) corneal and ocular surface repair – the most clinically mature domain, (2) cardiac tissue repair post-infarction, (3) dermal and cutaneous wound healing, and (4) broader systemic roles in inflammation and fibrosis modulation across liver, kidney, and colon tissue models (Xu et al., PMC8724243).
A critical methodological point for comparative researchers: because full-length Tβ4 (43 amino acids) and synthetic TB-500 (a shorter active-region fragment) are frequently conflated in secondary and tertiary literature, any comparative research design should explicitly specify which molecular entity is under investigation and cite primary sources accordingly, rather than assuming direct interchangeability of published Tβ4 findings with TB-500-specific study design.
Combined and Comparative Study Considerations
Researchers designing head-to-head or combination protocols involving BPC-157 and TB-500/Tβ4 should consider that the two compounds, despite overlapping downstream outcomes (angiogenesis, tissue repair acceleration), operate through non-redundant upstream mechanisms – VEGFR2/NOS/FAK signaling for BPC-157 versus direct actin-cytoskeletal regulation and ILK signaling for Tβ4. This mechanistic non-overlap is frequently cited as rationale in the peptide research community for combination study designs, though published, peer-reviewed data directly comparing or combining the two compounds in a single controlled study remains limited in the current PubMed-indexed literature. Researchers should treat any claims of synergy between these two peptides as hypothesis-generating rather than established, pending dedicated combination studies.
Future Directions in Research
Several open questions continue to drive active preclinical investigation for both compounds:
For BPC-157, ongoing research directions include further elucidation of the precise receptor or receptor-complex responsible for its pleiotropic effects (given the absence of a confirmed single high-affinity receptor), expanded neuroprotection studies in central nervous system injury models, and continued mechanistic dissection of its NO-system modulation, which appears to be bidirectional (protective versus cytotoxic NO signaling) depending on tissue context (Seiwerth et al., PMID 41155565).
For TB-500/Tβ4, research continues to focus on optimizing local delivery systems (such as the collagen-matrix controlled-release approaches already tested in cardiac models), further clinical-stage development of ocular formulations following the RGN-259 trial program, and clarification of which specific TB-4 sub-sequences are responsible for which discrete biological activities, building on early structure-function mapping work (Chiu et al., PMID 22817626; Xu et al., PMC8724243).
Both compounds also remain subjects of scoping and systematic review efforts aimed at consolidating the fragmented preclinical literature – a 2024 MDPI scoping review specifically flagged the need for more rigorously controlled, TB-500-specific (rather than general Tβ4) research to close the evidentiary gap between the parent molecule and its shorter synthetic research analog.
Conclusion
BPC-157 and TB-500 represent two of the most extensively referenced peptides in preclinical tissue-repair and regenerative biology research, yet they are mechanistically distinct compounds that should not be treated as interchangeable in research design or literature citation. BPC-157’s evidence base centers on a specific, well-characterized 15-amino-acid sequence with over 100 dedicated preclinical studies spanning gastrointestinal, musculoskeletal, and vascular research domains, converging on VEGFR2-mediated angiogenesis, NO-system modulation, and FAK-paxillin-dependent cell migration. TB-500’s evidence base is comparatively more indirect, drawing primarily from research on its parent molecule, full-length Thymosin Beta-4, which has produced a deep mechanistic literature on actin sequestration, ILK-mediated cardiac repair, and clinically advanced ocular applications, but comparatively sparse direct study of the shorter synthetic TB-500 fragment itself.
For researchers, the practical implication is clear: literature review and citation practices should carefully distinguish between compound-specific findings (BPC-157’s 15-mer sequence; TB-500’s active-region fragment) and parent-molecule findings (full Tβ4), and experimental designs comparing the two compounds should be built around their genuinely distinct upstream signaling mechanisms rather than assumed mechanistic equivalence based on overlapping downstream phenotypes such as “wound healing” or “angiogenesis.”
Core Research Peptides supplies BPC-157 and TB-500 as research-grade compounds intended solely for qualified laboratory and preclinical research applications. All compounds are provided strictly for research use only, are not for human or animal consumption, and are accompanied by applicable certificates of analysis for verification of purity and identity by the receiving research institution.
Frequently Asked Questions
Is BPC-157 the same compound as TB-500?
No. BPC-157 is a synthetic 15-amino-acid peptide derived from a gastric protective protein, while TB-500 is a synthetic peptide based on the active region of Thymosin Beta-4, a naturally occurring 43-amino-acid actin-binding protein. They have different amino acid sequences, different molecular origins, and operate through distinct primary mechanisms. Both are strictly research-use-only compounds and are not approved for human or veterinary therapeutic use.
Which compound has more published preclinical research: BPC-157 or TB-500?
BPC-157 has a larger body of compound-specific published preclinical literature, with over 100 dedicated studies using its exact sequence. TB-500-specific research is comparatively limited; most of the mechanistic and efficacy literature associated with the TB-500 name is derived from studies of its parent molecule, full-length Thymosin Beta-4, rather than the shorter synthetic fragment itself. Researchers should account for this distinction when designing studies or reviewing prior literature.
Do BPC-157 and TB-500 work through the same mechanism?
No, and this is a key research consideration. BPC-157’s mechanisms center on VEGFR2 receptor upregulation and internalization, nitric oxide (NO) system modulation, and FAK-paxillin-dependent cell migration signaling. TB-500/Thymosin Beta-4’s mechanism centers on direct G-actin sequestration, which regulates cytoskeletal dynamics required for cell migration, along with integrin-linked kinase (ILK) activation in cardiac tissue models. These are non-overlapping upstream pathways that happen to converge on some similar downstream outcomes, such as accelerated tissue repair in various preclinical models.
Has either compound been tested in human clinical trials?
Full-length Thymosin Beta-4 (the parent molecule of TB-500) has been studied in Phase 3 human clinical trials for dry eye syndrome and neurotrophic keratopathy under the designation RGN-259, representing an advanced clinical research program for the ocular application. This is distinct from TB-500 as sold for laboratory research use. BPC-157 has been studied in some published clinical contexts, including historical work related to inflammatory bowel disease, but the majority of the modern preclinical literature – and all Core Research Peptides product applications – pertain strictly to laboratory and animal research models, not approved human therapeutic use. Nothing in this article should be construed as evidence of safety or efficacy for human use of research-use-only compounds.
Are BPC-157 and TB-500 legal to purchase for research purposes?
Both compounds are available for purchase as research chemicals for use by qualified researchers, laboratories, and institutions, subject to applicable federal, state, and local regulations governing research chemical handling. They are not dietary supplements, are not intended for human consumption, and are not marketed or sold by Core Research Peptides for any therapeutic, diagnostic, or performance purpose. Purchasers are responsible for ensuring their use complies with all applicable research chemical regulations in their jurisdiction and institution.
Can BPC-157 and TB-500 be studied together in the same research protocol?
Because the two peptides operate through distinct, non-redundant upstream signaling mechanisms, some researchers have proposed combination study designs to investigate potential complementary or additive effects in tissue-repair models. However, dedicated, peer-reviewed, head-to-head or combination studies of BPC-157 and TB-500 remain limited in the current PubMed-indexed literature. Any research into combined administration should be treated as an open, hypothesis-generating question rather than one with an established evidentiary basis, and should follow appropriate institutional protocols for novel combination research.
Practical Guidance for Researchers Reviewing This Literature
Given the volume and heterogeneity of the published literature on both compounds, researchers new to this area may find it useful to approach the evidence base with a few organizing principles. First, always verify whether a given source paper studied the exact synthetic sequence marketed as “BPC-157” or “TB-500,” or whether it instead studied a related but distinct parent molecule – this distinction is especially important for TB-500, where the majority of indexed studies concern full-length Thymosin Beta-4 rather than the shorter synthetic fragment. Second, note the administration route and exposure regimen used in each preclinical study, since BPC-157 research in particular spans intraperitoneal, intramuscular, intragastric, topical, and oral drinking-water delivery methods across different disease models, each producing somewhat different pharmacokinetic and outcome profiles. Third, pay attention to species and injury model – rat tendon transection, rat gastric ulcer, and rat hind-limb ischemia models are not interchangeable, and effect sizes reported in one model should not be assumed to generalize to another tissue type or injury mechanism without dedicated study.
Researchers designing new preclinical protocols involving either compound should also consult institutional animal care and biosafety guidelines, since experimental use of research peptides in animal models is subject to standard laboratory animal welfare regulations (e.g., IACUC oversight in the United States) independent of any consideration of eventual translational potential. Sourcing of research compounds from a supplier with documented certificates of analysis and batch-specific purity testing is a baseline good-practice standard for any peptide research program, since inconsistent purity or identity is a well-recognized confound in reproducing preclinical peptide findings across laboratories.
Finally, researchers should remain attentive to the evolving scoping and systematic review literature summarizing this space. Because both BPC-157 and Thymosin Beta-4/TB-500 have generated a large volume of primary research spread across gastroenterology, orthopedics, cardiology, ophthalmology, and dermatology journals, periodic scoping reviews – such as the 2024 MDPI Applied Sciences review of Tβ4/TB-500 tissue-healing literature and the various Sikiric-group reviews of BPC-157’s pleiotropic effects – provide valuable consolidated entry points before diving into primary literature for a specific research question.
References
- Malinda KM, et al. Thymosin beta4 accelerates wound healing. J Invest Dermatol. 1999. PMID: 10469335
- Sosne G, et al. Thymosin beta 4 promotes corneal wound healing and decreases inflammation in vivo following alkali injury. Exp Eye Res. 2002. PMID: 11950239
- Chang CH, et al. Gastric pentadecapeptide BPC 157 accelerates healing of transected rat Achilles tendon and in vitro stimulates tendocytes growth. J Orthop Res. 2003. PMID: 14554208
- Xiao Y, et al. Protective effects of pentadecapeptide BPC 157 on gastric ulcer in rats. World J Gastroenterol. 2004. PMID: 15052688
- Bock-Marquette I, et al. Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair. Nature. 2004. PMID: 15565145
- Klicek R, et al. Achilles detachment in rat and stable gastric pentadecapeptide BPC 157: promoted tendon-to-bone healing and opposed corticosteroid aggravation. J Orthop Res. 2006. PMID: 16583442
- Goldstein AL, et al. Therapeutic potential of thymosin-beta4 and its derivative N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) in cardiac repair. Ann N Y Acad Sci. 2006. PMID: 17083265
- Mihaljevic V, et al. Gastric pentadecapeptide BPC 157 as an effective therapy for muscle crush injury in the rat. Surg Today. 2008. PMID: 18668315
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- Chiu LLY, et al. Controlled release of thymosin β4 from injected collagen-chitosan hydrogels promotes angiogenesis and prevents tissue loss after myocardial infarction. Regen Med. 2012. PMID: 22817626
- Sosne G, et al. Thymosin β4: a potential novel dry eye therapy. Ann N Y Acad Sci. 2012. PMID: 23050816
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- Quan Z, et al. Thymosin β4 promotes the survival and angiogenesis of transplanted endothelial progenitor cells in the infarcted myocardium. Int J Mol Med. 2017. PMID: 28440414
- Sosne G, et al. Thymosin beta 4 and the eye: the journey from bench to bedside. Expert Opin Biol Ther. 2018. PMID: 30063853
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- Sosne G, et al. Thymosin beta 4: a novel corneal wound healing and anti-inflammatory agent. PMC2701135
- Chang CH, et al. Pentadecapeptide BPC 157 Enhances the Growth Hormone Receptor Expression in Tendon Fibroblasts. PMC6271067
- Clopidogrel-Induced Gastric Injury in Rats is Attenuated by Stable Gastric Pentadecapeptide BPC 157. PMC7763470
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