Peptides for Healing: How Peptide Research Approaches Tissue Repair

Key Takeaways

• Compounds covered: BPC-157, TB-500 (thymosin beta-4 synthetic fragment), GHK-Cu (copper peptide)
• Goal area: Tissue repair and wound healing — musculoskeletal, dermal, post-surgical, and connective tissue recovery
• Evidence range: Ranges from extensive preclinical animal models across multiple tissue types (BPC-157, TB-500) to limited human wound healing data (thymosin beta-4) to in vitro and preclinical collagen synthesis evidence (GHK-Cu)
• Regulatory range: BPC-157 is on FDA's Category 2 list with FDA stating it does not support 503A compounding pending further review; TB-500 is not FDA-approved and has no lawful U.S. prescribing pathway; GHK-Cu is available as a topical cosmetic ingredient regulated under the FD&C Act, while injectable GHK-Cu is not FDA-approved, is not on the FDA 503A positive bulks list, and is not eligible for 503A compounding in the United States
• Key biomarkers for healing: hs-CRP (systemic inflammation baseline), IGF-1 (GH axis, relevant if secretagogues also considered), ALT/AST (liver safety), eGFR/creatinine (kidney function)
• As of April 2026: A 2025 systematic review in HSS Journal identified no completed human RCTs for BPC-157 in orthopedic applications; the compound remains on FDA's Category 2 list with FDA stating it does not support 503A compounding pending further agency review. This status is subject to change.
• Bottom line: Preclinical evidence for BPC-157 and TB-500 across tissue types is substantial; the absence of human RCTs means clinical conclusions for human healing applications cannot be drawn.

Tissue repair is one of the most studied areas in peptide research, and one of the clearest examples of the gap between preclinical promise and human clinical evidence. BPC-157 and thymosin beta-4 (the parent molecule of the peptide fragment sold in research-chemical channels as TB-500) have generated substantial animal-model data across wound healing, muscle repair, tendon healing, ligament recovery, and bone regeneration. GHK-Cu has shown collagen synthesis stimulation in cell culture and animal models. None of these compounds has completed a Phase 3 human clinical trial in any tissue repair indication.

That gap matters. It does not invalidate the preclinical science. But it does define what can and cannot be concluded from the existing evidence base.

Understanding Tissue Repair: The Biology

Tissue repair follows a conserved biological sequence across most tissue types: an inflammatory phase clears debris and signals cellular recruitment; a proliferative phase brings fibroblasts, endothelial cells, and tissue-specific progenitors to the injury site; a remodeling phase reorganizes new matrix into functional tissue. Each phase is time-dependent and regulated by distinct growth factors, cytokines, and cellular signals.

Vascularization is central to all phases. Without blood vessel formation — angiogenesis — repair cells cannot reach the injury site, metabolic waste cannot be cleared, and tissue growth cannot be sustained. This is why compounds with proposed angiogenic activity in preclinical models are mechanistically relevant to tissue repair research across all tissue types. Tendons and ligaments present a particular challenge: they are naturally hypovascular (poorly supplied with blood vessels), which is why their repair is slow and why angiogenic compounds have attracted attention in sports medicine research.

Growth factor signaling governs cellular behavior during repair. Vascular endothelial growth factor (VEGF) drives angiogenesis; fibroblast growth factors (FGFs) stimulate matrix-producing cells; transforming growth factor-beta (TGF-beta) governs collagen deposition. The growth hormone (GH) and IGF-1 axis intersects with repair through satellite cell activation in muscle, chondrocyte regulation in cartilage, and fibroblast stimulation in connective tissue. This is why IGF-1 — the primary bloodwork marker for GH axis activity — is a relevant baseline marker before considering any compound that intersects with this pathway.

Collagen is the structural material of repair. In tendons, ligaments, and dermis, Type I collagen is the primary matrix protein. In cartilage, Type II collagen predominates. Proper collagen organization — not just deposition, but cross-linking and fiber alignment — determines the functional quality of the healed tissue. Scar formation, by contrast, reflects disorganized collagen deposition that is structurally weaker than native tissue. Compounds that reduce scarring and promote organized matrix formation are therefore more relevant to functional recovery than those that simply accelerate raw collagen deposition.

Peptides Studied for Healing: A Quick Comparison

The following peptides have published evidence relevant to tissue repair. They are listed by strength of evidence, from most-studied to least. Evidence grading is explicit for each compound.

• Compound: BPC-157
  Mechanism for tissue repair: Angiogenesis via VEGFR2 upregulation; direct stimulation of tendon fibroblast outgrowth and survival; NO-system modulation; growth hormone receptor upregulation in repair cells
  Evidence: Extensive animal studies across wound, muscle, tendon, ligament, and bone injury models; one human IV safety pilot (2025); no completed human efficacy RCT in any tissue type
  FDA status: Not FDA-approved for any indication; on FDA's Category 2 list as of April 2026, with FDA stating it does not support 503A compounding pending further review (status subject to change)
  SP availability: Not offered through Superpower
  Route: Subcutaneous or intramuscular injection in animal studies; oral administration also studied in animals
• Compound: TB-500 (synthetic thymosin beta-4 fragment)
  Mechanism for tissue repair: Actin sequestration promoting cell migration; reduced myofibroblast differentiation limiting scar formation; extracellular matrix remodeling; angiogenesis; satellite cell recruitment in muscle
  Evidence: Animal studies across wound healing, muscle, ligament, and cardiac repair; one 2012 paper by Treadwell, Kleinman, and colleagues in the Annals of the New York Academy of Sciences included preclinical and limited human dermal repair data for full-length thymosin beta-4 (not the TB-500 fragment specifically); no human RCT for the TB-500 fragment
  FDA status: Not FDA-approved for any indication; not on the FDA 503A bulks list; no USP-NF monograph; not a component of any FDA-approved drug. Under Section 503A, TB-500 is not eligible for compounding. No FDA-approved TB-500 drug product exists. TB-500 has no lawful U.S. prescribing, dispensing, or compounding channel for human use.
  SP availability: Not offered through Superpower
  Route: Subcutaneous injection in research context
• Compound: GHK-Cu (glycyl-L-histidyl-L-lysine copper complex)
  Mechanism for tissue repair: Copper-mediated collagen synthesis stimulation in fibroblasts; anti-inflammatory signaling; angiogenesis promotion; gene expression changes toward tissue homeostasis
  Evidence: In vitro fibroblast studies; animal wound healing models; no human RCT for injectable GHK-Cu in tissue repair
  FDA status: As a topical cosmetic ingredient: regulated as a cosmetic under the FD&C Act (no drug claims); as a compounded injectable: not FDA-approved and not on the FDA 503A positive bulks list, has no USP-NF monograph, and is not a component of an FDA-approved drug — not eligible for 503A compounding. In April 2026, FDA additionally removed injectable GHK-Cu from its Category 2 interim bulks list without placing it on Category 1. Some compounding pharmacies have continued to prepare injectable GHK-Cu outside the 503A bulks framework; this activity carries FDA enforcement risk
  SP availability: Not offered through Superpower
  Route: Topical (cosmetic application); subcutaneous injection (compounded injectable, limited human use)

Compounds listed as research-only have not completed the clinical trial process required for FDA approval. TB-500 specifically has not been approved for human use and is not legal to prescribe or sell for human use in the US. Their inclusion here is for educational context only.

Peptides Studied for Healing: Individual Profiles

Each compound has a distinct mechanism and a distinct evidence record. They have been studied in different injury models, at different doses, and with different endpoints — direct comparison between them is not supported by the data.

BPC-157

BPC-157 is a synthetic 15-amino-acid peptide derived from a sequence in human gastric juice, studied extensively in animal models across multiple tissue types. It is not FDA-approved for any indication. As of April 2026, BPC-157 appears on FDA's Category 2 list of bulk drug substances; FDA has stated it does not support 503A compounding of this substance pending further agency review. This status is subject to change.

The primary healing mechanism involves angiogenesis through VEGFR2 upregulation. Hsieh and colleagues, writing in the Journal of Molecular Medicine in 2017, characterized BPC-157's pro-angiogenic activity via VEGFR2 activation, establishing the vascular mechanism that underlies its tissue-repair effects across organ systems. Seiwerth and colleagues, writing in Current Pharmaceutical Design in 2018, documented BPC-157's angiogenic mechanism across GI, tendon, ligament, muscle, and bone healing, demonstrating that the same vascular pathway drives repair activity in all connective tissue types.

For wound healing specifically, Seiwerth and colleagues in 2021 in Frontiers in Pharmacology reviewed BPC-157's wound healing effects including promotion of wound closure and angiogenesis in experimental models. Huang and colleagues, writing in Drug Design, Development and Therapy in 2015, demonstrated accelerated wound closure in alkali-burn animal models, promoting proliferation, migration, and angiogenesis in both in vivo and in vitro contexts. For muscle repair, Sikiric and colleagues published studies in the Journal of Orthopaedic Research in 2008 and 2010 documenting BPC-157's effects in crush injury and functional muscle repair models. Chang and colleagues, writing in the Journal of Applied Physiology in 2011, reported that BPC-157 supports tendon outgrowth and cell migration in animal tendon repair models. Cerovecki and colleagues in 2010 in the Journal of Orthopaedic Research documented BPC-157 effects in a rat ligament repair model. Matek and colleagues published a 2025 study in Pharmaceutics reporting that BPC-157 supported muscle-to-bone reattachment in a rat quadriceps detachment model, representing the most recent musculoskeletal repair data.

The state of human evidence was characterized by Vasireddi and colleagues in a 2025 systematic review in HSS Journal, which identified no completed human RCTs for BPC-157 in orthopedic sports medicine. The same finding was reinforced by McGuire and colleagues in a 2025 narrative review in Current Reviews in Musculoskeletal Medicine, which assessed BPC-157 musculoskeletal evidence while noting the absence of human trial data and unresolved safety concerns. A 2025 pilot study examined IV administration in humans, providing preliminary human safety and pharmacokinetic data, but not efficacy data for any healing indication.

[Animal study evidence across multiple tissue types; no completed human efficacy RCT]

Not available through Superpower. As of April 2026, no lawful U.S. compounding pathway exists for BPC-157 under Section 503A: it is not on the FDA 503A positive bulks list and has no FDA-approved drug product. This status is subject to change; readers should consult current FDA guidance.

TB-500 (synthetic thymosin beta-4 fragment)

TB-500 is a synthetic peptide fragment corresponding to a portion of thymosin beta-4, a naturally occurring 43-amino-acid protein that regulates actin polymerization and is expressed in virtually all mammalian cells. The term "TB-500" is used loosely in the research and supplement communities to refer to various thymosin beta-4 fragments (commonly described as either the Ac-SDKP tetrapeptide or a larger 17-amino-acid sequence; sources disagree). It is not FDA-approved. There is no FDA-approved TB-500 drug product that could be dispensed under a prescription, and TB-500 is not on the FDA 503A positive bulks list — meaning it has no lawful 503A compounding pathway. TB-500 therefore has no lawful U.S. prescribing, dispensing, or compounding channel for human use.

The primary healing mechanism — which TB-500 is proposed to share based on sequence homology — involves actin sequestration: by binding G-actin (monomeric actin), thymosin beta-4 increases the cellular pool of unpolymerized actin available for dynamic remodeling, which promotes cell migration — the foundational cellular behavior required for wound closure and tissue regeneration. The mechanistic studies cited below examined full-length thymosin beta-4 rather than the TB-500 fragment specifically. Malinda and colleagues, writing in the Journal of Investigative Dermatology in 1999, published foundational work reporting that thymosin beta-4 accelerated wound closure in animal models. Philp and colleagues, writing in Mechanisms of Ageing and Development in 2004, demonstrated thymosin beta-4 promotes angiogenesis, wound healing, and tissue repair across multiple contexts. Ehrlich and Hazard, writing in the Annals of the New York Academy of Sciences in 2010, documented thymosin beta-4's role in organizing connective tissue and preventing myofibroblast differentiation — the cellular pathway by which it is proposed to reduce scar formation. Philp and colleagues, writing in the Journal of Cellular Physiology in 2006, characterized thymosin beta-4's promotion of matrix metalloproteinase expression during wound repair, explaining its extracellular matrix remodeling mechanism. For muscle repair, Tokura and colleagues, in a 2011 study in the Journal of Biochemistry, demonstrated that muscle injury induces thymosin beta-4 expression, which acts as a chemoattractant for myoblasts, establishing the mechanism for satellite cell recruitment. Xu and colleagues, writing in Regulatory Peptides in 2013, documented thymosin beta-4 enhancement of medial collateral ligament healing in rat.

The most relevant human evidence involves full-length thymosin beta-4 rather than the TB-500 fragment. Treadwell, Kleinman, and colleagues, writing in the Annals of the New York Academy of Sciences in 2012, reported on thymosin beta-4 in dermal repair: preclinical and limited human data — representing one of the few contexts with any human tissue repair data. The distinction between the full-length protein and the TB-500 synthetic fragment is important: Ho and colleagues, writing in the Journal of Chromatography A in 2012, documented TB-500 as a synthetic fragment in equine anti-doping analysis, establishing the basis for its prohibition in sport.

[Animal studies with wound healing, muscle, and ligament data; limited human data specific to full-length thymosin beta-4, not the TB-500 fragment]

Not FDA-approved. Not on the FDA 503A positive bulks list. Not lawfully available through any licensed U.S. prescriber for any indication, and not available through Superpower. As of the 2026 WADA Prohibited List, thymosin beta-4 and its fragments are prohibited substances in sport.

GHK-Cu (glycyl-L-histidyl-L-lysine copper complex)

GHK-Cu is a naturally occurring human tripeptide complexed with copper(II) ions. It is found endogenously in plasma, urine, and saliva. As a topical cosmetic ingredient, it is regulated as a cosmetic under the FD&C Act and is available without a prescription. As a compounded injectable, GHK-Cu is not FDA-approved, is not on the FDA 503A positive bulks list, has no USP-NF monograph, and is not a component of an FDA-approved drug — under Section 503A, it is not eligible for compounding. In April 2026, FDA removed injectable GHK-Cu from its Category 2 interim bulks list without placing it on Category 1. Some compounding pharmacies have continued to prepare injectable GHK-Cu outside the 503A bulks framework; this activity carries FDA enforcement risk.

The primary mechanism relevant to tissue repair involves copper-mediated stimulation of collagen synthesis in fibroblasts. Maquart and colleagues, writing in FEBS Letters in 1988, published the seminal paper establishing that GHK-Cu stimulates collagen synthesis in fibroblast cultures — the foundational mechanistic evidence for its tissue repair applications. A follow-up in vivo study by Maquart and colleagues in the Journal of Clinical Investigation in 1993 confirmed connective tissue accumulation from GHK-Cu in animal models. Pickart and Margolina, writing in the International Journal of Molecular Sciences in 2018, published the most comprehensive review of GHK-Cu's mechanisms, documenting regenerative and protective effects across collagen synthesis, angiogenesis, anti-inflammatory signaling, and gene expression. Pickart, writing in the Journal of Biomaterials Science, Polymer Edition in 2008, provided a comprehensive overview of GHK-Cu's role in tissue remodeling. At the genomic level, Pickart and colleagues, writing in BioMed Research International in 2014, demonstrated that GHK-Cu alters gene expression patterns associated with tissue remodeling, including downregulation of inflammatory gene clusters.

[In vitro fibroblast studies and animal models; no human RCT for injectable GHK-Cu in tissue repair]

As a topical cosmetic ingredient: available OTC, not for medical claims. As a compounded injectable: not FDA-approved, not on the FDA 503A positive bulks list, no USP-NF monograph, and not a component of an FDA-approved drug — not eligible for 503A compounding. Not offered through Superpower.

Regulatory Status at a Glance

As of April 2026, the compounds discussed in this article carry the following regulatory statuses:

• BPC-157: Not FDA-approved for any indication. On FDA's Category 2 list of bulk drug substances as of April 2026; FDA has stated it does not support 503A compounding of BPC-157 pending further agency review. This status is subject to change.
• TB-500 (thymosin beta-4 synthetic fragment): Not FDA-approved for any indication. Not on the FDA 503A positive bulks list; no USP-NF monograph; not a component of any FDA-approved drug. Under Section 503A, TB-500 is not eligible for compounding. TB-500 has no lawful U.S. prescribing, compounding, or sales pathway for human use.
• GHK-Cu (topical): Regulated as a cosmetic ingredient under the FD&C Act; no drug approval; not evaluated by FDA to diagnose, treat, cure, or prevent disease.
• GHK-Cu (compounded injectable): Not FDA-approved, not on the FDA 503A positive bulks list, no USP-NF monograph, and not a component of an FDA-approved drug — not eligible for 503A compounding. In April 2026, FDA additionally removed injectable GHK-Cu from its Category 2 interim bulks list without placing it on Category 1.

Compounds listed as research-only or experimental are not legal to prescribe, compound, or sell for human use in the US. Their presence in this article is for educational context only.

Considerations When Comparing Peptides for Healing

Direct comparison between BPC-157, TB-500, and GHK-Cu is not supported by the existing evidence. They have been studied in different injury types, at different doses, in different animal models, and for different tissue targets. Inferring relative effectiveness from these separate preclinical studies is methodologically unreliable.

Tissue type and injury pattern: BPC-157 has the most comprehensive cross-tissue evidence base — wound healing, muscle, tendon, ligament, and bone have all been studied in separate animal models. TB-500's evidence is strongest in wound healing and connective tissue with a specific emphasis on reducing scar formation. GHK-Cu's evidence is concentrated in collagen synthesis stimulation, most relevant to skin and connective tissue applications.

Phase of repair: The inflammatory, proliferative, and remodeling phases of healing respond to different inputs. Angiogenic compounds like BPC-157 are most relevant to the early proliferative phase when vascular supply is being established. Matrix-remodeling effects attributed to TB-500 are more relevant to the later remodeling phase.

Evidence level: No compound in this article has human RCT efficacy data for tissue repair. The evidence base is preclinical. A provider evaluating these compounds will consider the quality and quantity of animal data, the mechanistic plausibility of the proposed effects, and the regulatory status of each compound.

Route and access: As of April 2026, no lawful 503A compounding pathway exists for BPC-157, TB-500, or injectable GHK-Cu in the US — none is on the FDA 503A positive bulks list. GHK-Cu as a topical cosmetic is accessible without a prescription. Some compounding pharmacies have prepared injectable GHK-Cu outside the 503A bulks framework; this activity carries FDA enforcement risk.

This is not an exhaustive list of clinical considerations. A licensed provider will evaluate your full health history, current medications, and baseline lab results before recommending any compound.

Safety Considerations

The safety profiles of BPC-157 and TB-500 in humans for tissue repair have not been characterized through adequate clinical trials. A 2025 human pilot study examined IV BPC-157 pharmacokinetics and acute safety in a small cohort without identifying acute concerns, but this study design does not generate the long-term safety data that Phase 3 trials would produce. TB-500 has no comparable human safety study for the synthetic fragment.

GHK-Cu as a topical ingredient has a well-characterized dermal safety profile from extensive cosmetic use. As a compounded injectable, peer-reviewed human safety data is minimal; the compound has not been evaluated in large-scale human clinical trials for tissue repair indications.

Sourcing from unregulated online vendors — products sold outside licensed pharmacy channels — carries contamination and dosing risks that cannot be mitigated by the end user. This is a sourcing-and-safety caution distinct from the patient-condition contraindications listed below.

Contraindications that apply broadly to tissue repair peptide therapy:

• Active or history of malignancy — angiogenic compounds carry theoretical concern regarding tumor vascularization; none of these compounds have been studied in cancer populations
• Pregnancy or breastfeeding — reproductive and developmental safety data does not exist for BPC-157 or TB-500
• Competitive athletes subject to anti-doping rules — as of the 2026 WADA Prohibited List, thymosin beta-4 and its fragments (including TB-500) are prohibited substances. BPC-157 is not a specifically named prohibited substance on the 2026 WADA Prohibited List but falls under the S0 non-approved substances category, which prohibits any pharmacological substance not currently approved by any governmental regulatory health authority for human therapeutic use

For compound-specific side effect profiles, see individual compound pages and consult a qualified healthcare provider.

What to Test Before Considering Peptides Studied for Healing

Regardless of which compound you and your provider discuss, baseline biomarker testing establishes a measurable starting point. Without it, there is no objective way to assess whether a compound is producing the expected physiological changes or whether those changes are beneficial. For tissue repair applications, the most directly relevant markers are inflammatory and growth hormone axis baselines, together with organ function markers for injectable compound safety.

• hs-CRP (high-sensitivity C-reactive protein): Measures systemic inflammatory burden. Why it matters for healing: active inflammation is part of the repair process, but chronic elevated inflammation impairs tissue remodeling. A baseline hs-CRP value distinguishes acute post-injury inflammation from chronic systemic inflammation and provides a reference point for tracking change over time.
• IGF-1 (insulin-like growth factor 1): Reflects GH axis activity. Why it matters: IGF-1 drives satellite cell activation in muscle, chondrocyte regulation, and fibroblast stimulation — all directly relevant to tissue repair. An IGF-1 baseline is particularly important if any GH-secretagogue compound is also under consideration alongside BPC-157 or TB-500.
• ALT (alanine aminotransferase): Liver enzyme marker. Why it matters: any injectable compound undergoes hepatic processing, and a pre-treatment ALT baseline identifies pre-existing liver enzyme elevation that would confound interpretation of any subsequent changes.
• AST (aspartate aminotransferase): A second liver enzyme. Why it matters: ALT and AST together provide a more complete hepatic safety baseline for any injectable compound or intervention.
• eGFR (estimated glomerular filtration rate): Measures kidney filtration function. Why it matters: renal clearance affects how injectable peptides are processed. A pre-treatment eGFR value is a standard safety assessment for any injectable compound protocol.
• Comprehensive metabolic panel: Covers liver enzymes, kidney function, electrolytes, glucose, and protein markers in a single draw — the most efficient way to establish the organ-function baseline relevant to any injectable compound.

These markers do not directly measure tissue repair progress — imaging, functional testing, and physical examination are the tools for that. But they establish the objective safety and biological context that makes any intervention data interpretable. Markers most relevant to recovery contexts are covered in the inflammation and recovery biomarker guide.

How These Compounds Are Accessed

As of April 2026, no lawful U.S. compounding pathway exists for BPC-157 or TB-500 under Section 503A: neither substance is on the FDA 503A positive bulks list, and neither has an FDA-approved drug product. BPC-157 is on FDA's Category 2 list with FDA stating it does not support 503A compounding pending further review; TB-500 has no FDA-recognized compounding pathway and no FDA-approved indication. GHK-Cu as a topical cosmetic is available OTC; injectable GHK-Cu is not FDA-approved, is not on the FDA 503A positive bulks list, has no USP-NF monograph, and is not a component of an FDA-approved drug — under Section 503A, it is not eligible for compounding. In April 2026, FDA additionally removed injectable GHK-Cu from its Category 2 interim bulks list without placing it on Category 1.

For anyone recovering from injury or surgery, the primary access pathway for evidence-based care is clinical: an orthopedist, physical therapist, or sports medicine physician can evaluate the specific injury, recommend the appropriate standard-of-care interventions (which have substantially stronger human evidence than the compounds in this article), and identify whether any emerging compound is appropriate for their specific clinical context.

Products sold online as injectable BPC-157 or TB-500 operate outside pharmaceutical manufacturing oversight. Independent testing of gray-market peptide products has found contamination, incorrect dosing, and misidentified compounds. A clinical evaluation before considering any compound in this category is the appropriate starting point.

Understanding Your Baseline

With multiple compounds proposed for tissue repair — each targeting different mechanisms in the healing cascade, each with a different evidence profile — baseline biomarker data is what converts "which compound should I try?" into a conversation grounded in your specific biology. An IGF-1 level, a CRP measurement, and an organ function baseline are objective data points that a provider can use to evaluate any compound's relevance to your situation.

That principle — test first, then decide — is central to Superpower's approach to preventive health. Whether the conversation with your provider leads to a standard-of-care rehabilitation protocol, a compounded formulation, or a clinical trial, the starting point is the same: knowing where your biomarkers stand.

IMPORTANT SAFETY INFORMATION

BPC-157 is not approved by the FDA for any medical use. Research on BPC-157 has been limited primarily to laboratory and animal studies, with minimal human clinical trial data available. Its safety, efficacy, appropriate dosing, and long-term effects in humans have not been established. As of April 2026, BPC-157 appears on FDA's Category 2 list of bulk drug substances; FDA has stated it does not support 503A compounding of this substance pending further agency review. This regulatory status is subject to change; readers should consult current FDA guidance. BPC-157 is not prescribed, compounded, or dispensed through Superpower. This page is provided for educational purposes only and does not constitute medical advice or an endorsement of use.

TB-500 (synthetic thymosin beta-4 fragment) is not approved by the FDA for any medical use. Research is limited primarily to laboratory and animal studies. Safety, efficacy, appropriate dosing, and long-term effects in humans have not been established. TB-500 is not legal to prescribe, compound, or sell for human use in the US. It is not prescribed, compounded, or dispensed through Superpower. As of the 2026 WADA Prohibited List, thymosin beta-4 and its fragments are prohibited substances in sport. Inclusion in this article is for educational purposes only.

GHK-Cu (glycyl-L-histidyl-L-lysine copper complex): As a topical cosmetic ingredient, GHK-Cu is regulated as a cosmetic under the FD&C Act. Cosmetic ingredients are not evaluated or approved to diagnose, treat, cure, or prevent any disease or medical condition. As a compounded injectable, GHK-Cu is not FDA-approved for any indication, is not on the FDA 503A positive bulks list, has no USP-NF monograph, and is not a component of an FDA-approved drug — under Section 503A, it is not eligible for compounding. In April 2026, FDA removed injectable GHK-Cu from its Category 2 interim bulks list without placing it on Category 1. Injectable GHK-Cu is not prescribed, compounded, dispensed, or otherwise facilitated through Superpower.

This content is not a substitute for medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider before starting any peptide therapy. Individual health conditions, medications, and organ function affect both suitability and response.

The compounds discussed on this page do not have FDA-approved prescribing information available at DailyMed because none are FDA-approved.