Peptides for Tendon Repair: BPC-157, TB-500, and the Evidence on Tendonitis Recovery

Key Takeaways

• Compounds covered: BPC-157, TB-500 (thymosin beta-4 synthetic fragment), GHRP-2 (growth hormone-releasing peptide 2)
• Goal area: Tendon repair and tendonitis recovery — including Achilles tendinopathy, rotator cuff injury, patellar tendinopathy, and post-surgical tendon-to-bone reattachment
• Evidence range: Multiple independent Achilles and quadriceps tendon animal studies (BPC-157); connective tissue and ligament animal data with mechanistic relevance to tendons (TB-500); single rotator cuff animal model (GHRP-2); no completed human RCT for any compound in tendon repair
• Regulatory range: BPC-157 is not FDA-approved and, following FDA's February 2026 removal from the Category 2 interim bulks list, has no recognized 503A compounding pathway; TB-500 is not FDA-approved and is not legal to prescribe, compound, or sell for human use in the US; GHRP-2 is not FDA-approved and is not on FDA's positive 503A bulks list, though some 503A pharmacies have historically compounded it under patient-specific prescriptions
• Key biomarkers for tendon repair: hs-CRP (systemic inflammation), IGF-1 (GH axis baseline), ALT/AST (liver safety), eGFR (kidney function)
• As of April 2026: No peptide is FDA-approved for tendon repair or tendonitis. A 2025 systematic review confirmed no completed human RCTs for BPC-157 in orthopedic sports medicine.
• Bottom line: BPC-157 has a substantial, tendon-specific preclinical evidence base including multiple independent Achilles tendon studies; the absence of human RCTs means the animal evidence cannot yet be translated into clinical conclusions.

Tendons are biologically challenging structures. They are load-bearing cords of densely organized collagen that transmit muscle force to bone — and they are among the most poorly vascularized tissues in the body. The Achilles tendon, patellar tendon, and rotator cuff tendons are the sites of most clinical tendinopathy, partly because their hypovascular nature slows cellular repair to a fraction of the speed seen in well-vascularized tissues. The standard clinical toolkit for tendon injuries — eccentric loading, physiotherapy, corticosteroid injections, PRP, and surgery for severe cases — produces inconsistent results, particularly in chronic tendinopathy where the pathological tissue has undergone degenerative remodeling rather than active inflammation.

This clinical frustration is part of why peptides like BPC-157 attract serious attention in sports medicine research. The biological rationale — angiogenic stimulation of a hypovascular tissue, combined with direct fibroblast activation — maps onto the known limitations of tendon healing in a mechanistically coherent way. Whether that coherent mechanism translates to clinical benefit in people remains to be established by human trials that have not yet been completed.

Understanding Tendon Repair: The Biology

Tendon tissue is composed primarily of type I collagen fibers organized in a parallel hierarchical structure: collagen molecules aggregate into fibrils, fibrils form fibers, and fibers are organized into fascicles bound by endotenon sheaths. Tendocytes (tendon fibroblasts) maintain this matrix in a low-turnover steady state; injury disrupts the organization and triggers repair through the inflammatory-proliferative-remodeling sequence common to all connective tissues.

The challenge is that the remodeling phase in tendons is slow — weeks to months — and frequently produces mechanically inferior type III collagen (scar) before the tissue transitions to organized type I collagen. Jaschke and colleagues, writing in Cell and Tissue Research in 2026, provided a tendon physiology and healing overview, establishing that the natural repair sequence involves matrix metalloproteinase-driven remodeling of provisional scar matrix into organized load-bearing tissue over 12 or more weeks. Hammerman and colleagues, writing in the Journal of Applied Physiology in 2017, showed phase-dependent gene response to loading in Achilles tendon healing — a finding with implications for how timing of mechanical loading (and potentially of biologically active compounds) interacts with repair phase.

Vascularization is the central limiting factor. Tendons receive their blood supply primarily at the musculotendinous junction and at the osteotendinous (tendon-to-bone) insertion — leaving the mid-substance relatively avascular. This is why tendon mid-substance injuries heal slowly and why angiogenic compounds that stimulate new vessel formation in tendon tissue are mechanistically relevant. It also explains the interest in the osteotendinous junction: BPC-157's documented effects at that interface are directly relevant to rotator cuff and Achilles tendon pathology.

Legrand and colleagues, writing in the Journal of Hand Surgery in 2017, reviewed flexor tendon healing biology and strategies to reduce peritendinous adhesions, documenting that excessive scar formation and peritendinous adhesion are primary causes of post-tendon-surgery dysfunction. Any compound that reduces scar formation while supporting organized matrix deposition is therefore relevant to post-surgical outcomes, not just to acute injury healing.

Positioning peptide therapy in context: Chalidis and colleagues, writing in the International Journal of Molecular Sciences in 2023, reviewed PRP's effects in tendon healing — establishing PRP as the most-studied biological regenerative intervention in this space, with a comparatively more robust human evidence base than BPC-157 or TB-500.

Peptides Studied for Tendon Repair: A Quick Comparison

The following peptides have published evidence relevant to tendon repair. Listed by strength of tendon-specific evidence, from most-studied to least.

• Compound: BPC-157
  Mechanism for tendon repair: Tendocyte stimulation — outgrowth, survival, and directed migration; angiogenesis via VEGFR2; GH receptor upregulation in tendon fibroblasts; anti-nociceptive effects reducing pain; osteotendinous junction repair
  Evidence: Multiple independent Achilles tendon animal studies (transection, detachment, functional recovery models); in vitro tendocyte and fibroblast studies; animal quadriceps and myotendinous junction studies; early human pharmacokinetic/safety data reported in the 2025 Vasireddi et al. systematic review; no human tendon efficacy RCT
  FDA status: Not FDA-approved; removed from FDA's Category 2 interim bulks list in February 2026 and not on the approved 503A bulks list — no recognized 503A compounding pathway
  SP availability: Not currently available through Superpower
  Route: Subcutaneous or intramuscular injection in animal studies; local injection also studied
• Compound: TB-500 (synthetic thymosin beta-4 fragment)
  Mechanism for tendon repair: Actin sequestration promoting tendocyte migration; myofibroblast reduction limiting peritendinous adhesion; extracellular matrix remodeling; angiogenesis supporting hypovascular tendon tissue
  Evidence: Animal connective tissue and ligament healing studies; anti-fibrotic data in tissue injury models; no tendon-specific human RCT
  FDA status: Not FDA-approved; not on FDA's 503A bulks list; not legal to prescribe, compound, or sell for human use in the US
  SP availability: Not currently available through Superpower
  Route: Subcutaneous injection in research context
• Compound: GHRP-2 (growth hormone-releasing peptide 2)
  Mechanism for tendon repair: GH secretagogue activity — stimulates pituitary GH release; reduced M1 macrophage pro-inflammatory polarization at tendon-bone interface; improved tendon-to-bone histology in early repair
  Evidence: One rat rotator cuff animal model from Li and colleagues in 2025; no human RCT
  FDA status: Not FDA-approved; not on FDA's positive 503A bulks list. Some 503A pharmacies have historically compounded GHRP-2 under patient-specific prescriptions; FDA has not affirmed this practice and access varies by state and pharmacy
  SP availability: Not currently available through Superpower
  Route: Subcutaneous injection in research context

Compounds that are not FDA-approved and not on FDA's positive 503A bulks list have not completed the clinical trial process required for FDA approval. TB-500 is not legal to prescribe, compound, or sell for human use in the US. Their inclusion here is for educational context only.

Peptides Studied for Tendon Repair: Individual Profiles

Each compound has a distinct mechanism and distinct evidence base. They are not interchangeable, and their evidence bases are not directly comparable.

BPC-157

BPC-157 is a synthetic 15-amino-acid pentadecapeptide with a substantial, tendon-specific preclinical evidence base. It is not FDA-approved. It does not satisfy any of the three statutory criteria for lawful 503A compounding under 21 U.S.C. § 353a(b)(1)(A): it is not on FDA's positive 503A bulks list, has no USP monograph, and is not a component of any FDA-approved drug. Following FDA's February 2026 action removing BPC-157 from the Category 2 interim bulks list — which had reflected pending safety review rather than affirmative 503A eligibility — licensed 503A pharmacies do not have a recognized pathway to compound BPC-157 for human use. Removal from the Category 2 interim list does not equate to Category 1 eligibility.

The foundational tendon evidence comes from a landmark 2003 study by Staresinic and colleagues in the Journal of Orthopaedic Research, which reported BPC-157 accelerated rat Achilles tendon repair and stimulated tendocyte growth in vitro — establishing both the in vivo repair effect and the cellular mechanism of tendon fibroblast stimulation. Krivic and colleagues, writing in the Journal of Orthopaedic Research in 2006, reported BPC-157 effects on tendon-to-bone healing after Achilles detachment in rats and, critically, found that it opposed corticosteroid-induced tendon aggravation — a finding directly relevant to the clinical concern about corticosteroid injections weakening tendon tissue. A follow-on study by Krivic and colleagues in Inflammation Research in 2008 documented BPC-157 early Achilles tendon-to-bone recovery, characterizing the timeline of benefit in the early inflammatory repair phase. Chang and colleagues, writing in the Journal of Applied Physiology in 2011, reported BPC-157 effects on tendocyte biology — outgrowth, cell survival, and directed cell migration — in human and animal tendon fibroblasts. Chang and colleagues, writing in Molecules in 2014, reported BPC-157 effects on GH receptor expression in tendon fibroblasts, providing a molecular link to the GH/IGF-1 axis that governs connective tissue anabolism. Brcic and colleagues, writing in the Journal of Physiology and Pharmacology in 2009, documented BPC-157's angiogenic effects via VEGF in muscle and tendon, establishing the vascular mechanism directly relevant to hypovascular tendon tissue. Japjec and colleagues in 2021 documented BPC-157 at disabled myotendinous junctions, relevant to tendon-to-muscle attachment pathology. The most recent anatomical evidence comes from Matek and colleagues, writing in Pharmaceuticals in 2026, who reviewed BPC-157 at musculoskeletal injury sites including the osteotendinous junction — the interface critical in rotator cuff and Achilles pathology.

The broader musculoskeletal evidence synthesis was provided by Gwyer and colleagues' 2019 review in Cell and Tissue Research, which reviewed BPC-157 musculoskeletal soft tissue effects, with particular emphasis on tendon across multiple animal injury models. This context was updated by the 2025 systematic review by Vasireddi and colleagues in the HSS Journal, which identified no completed human RCTs despite the substantial animal evidence base and summarized a separately published small IV pharmacokinetic/safety pilot in its evidence review. DeFoor and colleagues, writing in Arthroscopy in 2025, contextualized BPC-157 within regenerative medicine research for sports performance. For pain alongside structural repair, Jung and colleagues in 2022 documented BPC-157 anti-nociceptive effects in a small rat incisional pain model that reported short-duration phase-1-only antinociceptive effects. Yuan and colleagues, writing in the International Journal of Molecular Sciences in 2026, reviewed BPC-157 tissue repair and analgesia roles.

For clinical framing, Mayfield and colleagues, writing in The American Journal of Sports Medicine in 2026, published a sports medicine peptide primer, acknowledging BPC-157's preclinical evidence base while emphasizing the absence of human RCT data. Mendias and colleagues, writing in Sports Medicine in 2026, reviewed unapproved peptide safety and efficacy gaps in musculoskeletal injuries, noting that rigorous human safety data remain scarce despite favorable preclinical profiles.

[Multiple independent animal Achilles and tendon-to-bone studies; in vitro tendocyte work; early human pharmacokinetic/safety data reported in the 2025 Vasireddi et al. systematic review; no completed human tendon efficacy RCT]

Not available through Superpower. BPC-157 does not satisfy any of the three statutory criteria for lawful 503A compounding under 21 U.S.C. § 353a(b)(1)(A), and following FDA's February 2026 removal of BPC-157 from the Category 2 interim bulks list, licensed 503A pharmacies do not have a recognized pathway to compound it for human use. It is not FDA-approved for any indication.

TB-500 (synthetic thymosin beta-4 fragment)

TB-500 is a synthetic thymosin beta-4 fragment with mechanisms relevant to tendon repair primarily through actin regulation and connective tissue remodeling. Its tendon-specific evidence is less direct than BPC-157's — most relevant data is from connective tissue and ligament healing models — but the mechanisms are coherent with tendon biology. It is not FDA-approved, is not on FDA's 503A bulks list, and is not legal to prescribe, compound, or sell for human use in the US.

The actin-sequestration mechanism is the primary driver of TB-500's relevance to tendons. Tendon fibroblast migration — essential for repair — requires cytoskeletal remodeling governed by actin dynamics. Bjorklund and colleagues, writing in Current Medicinal Chemistry in 2020, reviewed thymosin beta-4's tissue repair properties in the context of cardiac injury, with mechanistic relevance (anti-fibrotic, anti-inflammatory) also applicable to tendon biology — the anti-fibrotic aspect being particularly relevant to preventing peritendinous adhesion after repair. Dube and colleagues, writing in Expert Opinion on Biological Therapy in 2018, reviewed thymosin beta-4 vascular and tissue repair roles, including angiogenic contributions to hypovascular tendon tissue.

The peritendinous adhesion problem is a specific post-surgical concern: excessive scarring after tendon repair surgery restricts gliding and impairs function. Any compound that reduces myofibroblast-driven scar formation during tendon healing has clinical relevance in this context. TB-500's anti-myofibroblast evidence in connective tissue models is mechanistically relevant here, though tendon-specific data is limited.

[Connective tissue and ligament animal studies; mechanistically relevant to tendons but limited tendon-specific data; no human tendon RCT]

Not FDA-approved. Not on FDA's 503A bulks list. Not legal to prescribe, compound, or sell for human use in the US. As of the 2026 WADA Prohibited List, thymosin beta-4 and its fragments are prohibited substances in sport.

GHRP-2

GHRP-2 (growth hormone-releasing peptide 2) is a synthetic hexapeptide GH secretagogue that stimulates the pituitary gland to release endogenous growth hormone. It is not FDA-approved for any indication and is not on FDA's positive 503A bulk drug substances list. Some 503A pharmacies have historically compounded GHRP-2 under patient-specific prescriptions; FDA has not affirmed this practice, and access remains subject to enforcement discretion and varies by state and pharmacy.

Its relevance to tendon repair comes from GH and IGF-1 axis activity at the tendon-bone interface. Li and colleagues, writing in Arthroscopy in 2025, reported GHRP-2 rat rotator cuff findings, including decreased M1 macrophage production and histological changes at the tendon-bone interface — a direct published preclinical link between a GH secretagogue and tendon-to-bone repair. The mechanism involves both reduced pro-inflammatory macrophage polarization at the repair site and anabolic signaling from GH and downstream IGF-1. Mendoza Mari and colleagues, writing in Plastic Surgery International in 2016, documented GHRP-6 wound healing effects in a human study — establishing a general tissue-healing mechanism for GH-releasing peptides that complements BPC-157 in connective tissue repair contexts. Chang and colleagues' 2014 BPC-157 work showed GH receptor upregulation in tendon fibroblasts — suggesting that BPC-157 and GH secretagogues like GHRP-2 may act through partially convergent pathways in tendon fibroblasts.

[Single animal rotator cuff model (2025); general wound healing data for GH-releasing peptides; no human tendon RCT]

Not FDA-approved and not on FDA's positive 503A bulks list. Some 503A pharmacies have historically compounded GHRP-2 under patient-specific prescriptions; the regulatory status under Section 503A remains unsettled. Not currently available 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. It does not satisfy any of the three statutory criteria for lawful 503A compounding under 21 U.S.C. § 353a(b)(1)(A): not on FDA's positive 503A bulks list, no USP monograph, and not a component of any FDA-approved drug. Following FDA's February 2026 action removing BPC-157 from the Category 2 interim bulks list, licensed 503A pharmacies do not have a recognized pathway to compound it for human use. Removal from Category 2 does not equate to Category 1 eligibility.
• TB-500 (thymosin beta-4 synthetic fragment): Not FDA-approved for any indication. Not on FDA's 503A bulks list and not legal to prescribe, compound, or sell for human use in the US. Prohibited under the 2026 WADA Prohibited List.
• GHRP-2: Not FDA-approved for any indication. Not on FDA's positive 503A bulks list. Some 503A pharmacies have historically compounded GHRP-2 under patient-specific prescriptions; FDA has not affirmed this practice, and access varies by state and pharmacy. Its use for tendon repair is off-label and not supported by adequate clinical trial evidence.

Compounds that are not FDA-approved and not on a recognized 503A compounding pathway 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 Tendon Repair

Direct comparison between these compounds for tendon repair is not supported by the evidence. BPC-157 has multiple tendon-specific animal studies; TB-500 has connective tissue evidence that is mechanistically relevant but less tendon-specific; GHRP-2 has a single animal tendon-to-bone study. These different evidence foundations cannot be reconciled into a comparative efficacy judgment.

Injury type and tendon location: Achilles tendinopathy has the most BPC-157 animal data; rotator cuff pathology has GHRP-2 animal data; patellar tendinopathy has neither. A provider evaluating these compounds will map the proposed mechanism onto the specific injury location and type.

Phase of injury: Acute tendon tear, subacute recovery, and chronic tendinopathy are biologically distinct phases with different dominant processes. Angiogenic compounds like BPC-157 are most relevant when insufficient vascularization is limiting repair. Anti-fibrotic compounds like TB-500 are most relevant when scar formation and adhesion are the predominant concerns. A provider will evaluate which phase of injury you are in.

Rehabilitation context: Hammerman and colleagues' data on load-timing effects on Achilles tendon gene expression suggests that the timing of biological interventions relative to mechanical loading matters. Peptide therapy, if considered, would be evaluated in the context of the complete rehabilitation program — not as a substitute for it. Mendias and colleagues' 2026 review emphasizes that compounds in this category should be considered as potential adjuncts to established rehabilitation, not replacements.

Regulatory access: As of April 2026, of the three compounds discussed, only GHRP-2 has any practical access pathway — through licensed prescribers at some 503A compounding pharmacies — but the regulatory status under Section 503A remains unsettled and FDA has not affirmed this practice. BPC-157 was removed from the Category 2 interim bulks list in February 2026 and has no recognized 503A compounding pathway; TB-500 is not legal to prescribe, compound, or sell for human use. Any injectable BPC-157 or TB-500 sold online operates outside regulated manufacturing.

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 for tendon repair have not been characterized through adequate human clinical trials. The 2025 Vasireddi et al. systematic review (HSS Journal) summarizes a separately published small IV pharmacokinetic/safety pilot in its evidence table; the pilot itself is not a substitute for the randomized, adequately powered safety data FDA approval requires, and it does not constitute a long-term tendon safety profile. TB-500 has no comparable human safety study. GHRP-2's safety profile in the context of tendon repair specifically has not been characterized; its general GH-secretagogue class effects include potential IGF-1 elevation which warrants monitoring.

Contraindications that apply broadly to tendon repair peptide therapy:

• Active infection at or near the tendon — any injectable compound is contraindicated in the presence of local infection; septic tenosynovitis requires urgent clinical management
• Active or history of hormone-sensitive malignancy — angiogenic compounds carry theoretical concern regarding tumor vascularization; GH secretagogues carry additional consideration for IGF-1-sensitive malignancies
• Pregnancy or breastfeeding — reproductive safety data does not exist for any compound in this article
• Competitive athletes subject to anti-doping rules — TB-500 (synthetic thymosin beta-4 fragment) is explicitly prohibited under Section S2 of the 2026 WADA Prohibited List; GHRP-2 is explicitly prohibited under Section S2 as a growth hormone secretagogue; BPC-157 is not specifically enumerated on the 2026 List but is generally captured under WADA's S0 "Non-Approved Substances" category, which prohibits pharmacological substances not currently approved by any governmental regulatory authority for human therapeutic use. Athletes should verify current status with their national anti-doping agency before any use
• Products from unregulated online sources — injectable products sold outside licensed pharmacy channels carry contamination and dosing risks that cannot be mitigated by the end user

For compound-specific safety data, consult individual compound literature and a licensed healthcare provider familiar with your injury history.

What to Test Before Starting Peptides for Tendon Repair

Regardless of which compound you and your provider discuss, baseline biomarker testing establishes the biological context before any intervention. For tendon repair applications, the most directly relevant markers cover systemic inflammation, growth hormone axis activity, and organ function safety baselines for injectable compounds.

• hs-CRP (high-sensitivity C-reactive protein): Measures systemic inflammatory burden. Why it matters for tendon repair: persistent elevated systemic inflammation impairs the remodeling phase of tendon repair. A baseline hs-CRP value characterizes the inflammatory context before any intervention and establishes a reference for tracking change.
• IGF-1 (insulin-like growth factor 1): Reflects GH axis activity directly relevant to connective tissue anabolism. Why it matters: BPC-157 has been shown to upregulate GH receptor expression in tendon fibroblasts, and GHRP-2 stimulates GH release — making IGF-1 the primary monitoring marker for any compound that intersects with the GH/IGF-1 axis. An IGF-1 baseline is essential before any GH-secretagogue is considered.
• ALT (alanine aminotransferase): Liver enzyme safety baseline for injectable compounds. A pre-treatment ALT value establishes hepatic health context before any injectable protocol.
• eGFR (estimated glomerular filtration rate): Kidney filtration function. An eGFR baseline is standard pre-treatment assessment for any injectable compound — renal clearance affects pharmacokinetics and monitoring thresholds.
• Comprehensive metabolic panel: Covers liver enzymes, kidney function, glucose, and electrolytes in a single draw — the most efficient organ-function baseline for any injectable compound protocol.

These markers do not directly measure tendon structure or repair progress — MRI, diagnostic ultrasound, and clinical functional testing are the tools for that assessment. But they establish the objective biological context that makes any intervention interpretable and supports the clinical conversation about what approach is appropriate for your specific injury.

How to Access These Peptides Safely

As of April 2026, BPC-157 and TB-500 do not satisfy any of the three statutory criteria for lawful 503A compounding under 21 U.S.C. § 353a(b)(1)(A) and do not have a recognized 503A compounding pathway in the US. GHRP-2 is accessible through licensed prescribers at some 503A compounding pharmacies; the regulatory status under Section 503A remains unsettled and FDA has not affirmed this practice. Any injectable product sold online as BPC-157 or TB-500 operates outside FDA manufacturing oversight.

For anyone managing a tendon injury, the appropriate starting point is sports medicine or orthopedic evaluation. A sports medicine physician, orthopedic surgeon, or physical therapist can characterize the injury precisely — distinguishing tendon tear from tendinopathy from peritendinous adhesion — and recommend the evidence-based rehabilitation approach for the specific pathology. Eccentric loading programs, physical therapy, and in selected cases PRP or surgery have substantially more human evidence than the compounds in this article. The clinical conversation about whether any emerging compound is appropriate begins after the diagnosis is established, not before.

Products sold online as injectable tendon-repair peptides are not regulated for identity, purity, or dosing. Contamination and dosing inconsistency are documented risks in this product category. A prescription from a licensed provider who has evaluated your injury and ordered baseline labs is the minimum standard for any injectable protocol.

Understanding Your Baseline

Tendon injuries are among the most variable in recovery time, response to intervention, and long-term outcome — and much of that variability is biological. Knowing your IGF-1 status, systemic inflammatory burden, and organ function before considering any compound gives a provider the objective context to evaluate whether any intervention is appropriate and to track whether it is producing the expected changes.

That principle is central to Superpower's approach to preventive health. Whether the clinical conversation leads to a structured rehabilitation program, a compounded formulation from a licensed prescriber, or continued evaluation, 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 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. It does not satisfy any of the three statutory criteria for lawful 503A compounding under 21 U.S.C. § 353a(b)(1)(A): it is not on FDA's positive 503A bulks list, has no USP monograph, and is not a component of any FDA-approved drug. Following FDA's February 2026 action removing BPC-157 from the Category 2 interim bulks list — which had reflected pending safety review rather than affirmative 503A eligibility — licensed 503A pharmacies do not have a recognized pathway to compound BPC-157 for human use. Removal from the Category 2 interim list does not equate to Category 1 eligibility. BPC-157 is not prescribed, compounded, or dispensed through Superpower. This page is 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 to laboratory and animal studies. Safety, efficacy, appropriate dosing, and long-term effects in humans have not been established. TB-500 is not on FDA's 503A bulks list and 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.

GHRP-2 (growth hormone-releasing peptide 2) is not FDA-approved for any indication. Its use for tendon repair has not been evaluated or endorsed by the FDA. Compounded GHRP-2 is not the same as an FDA-approved product. GHRP-2 is prohibited under Section S2 of the 2026 WADA Prohibited List as a growth hormone secretagogue. It is not currently available through Superpower. This page is for educational purposes only and does not constitute medical advice or a recommendation to use this compound.

This content is not a substitute for medical advice, diagnosis, or treatment. Tendon injuries require clinical evaluation. Always consult a qualified sports medicine physician or orthopedic provider before starting any compound. Individual health conditions, medications, and injury severity affect both suitability and response.

Full FDA-approved prescribing information at dailymed.nlm.nih.gov.