BPC-157
Body Protection Compound-157 (BPC-157)
Strong tissue repair peptide with zero evidence for hair loss — a category error when applied to the scalp.
How BPC-157 works — and how well we know it
BPC-157 is a synthetic 15-amino acid peptide derived from a protein found in human gastric juice. It promotes tissue repair primarily through upregulation of VEGFR2 (a blood vessel growth receptor), activation of the FAK-paxillin cell migration pathway, and modulation of nitric oxide synthesis. It has no demonstrated activity on any hair-loss-specific pathway.
oral, injection, topical, subcutaneous injection
No established dosing for hair loss. In preclinical studies, doses range from 6 µg/kg to 20 mg/kg across multiple routes. No human dosing guidance exists for any indication.
No regulatory approval for any indication. A Phase II trial for ulcerative colitis (PL14736) was conducted in Croatia but full results were never published.
Gut healing and musculoskeletal tissue repair (preclinical only). Not a hair loss treatment.
Evidence distribution across 8 claims
Why the grade is D. Zero published studies on BPC-157 and hair growth in any model. No mechanism overlap with androgenetic alopecia pathways (DHT, Wnt/beta-catenin, follicle miniaturization). Preclinical tissue repair evidence is strong but entirely irrelevant to hair biology.
What the studies actually showed
Unknown for hair (no data exists). For tissue repair in animal models, effects are typically observed within days to weeks depending on the injury model. Self-experimenters who claim hair benefits typically report waiting 2-4 months, but this timeline is indistinguishable from placebo or concurrent treatment effects.
Unknown for hair (no data exists). No dose-response curve has been established for any hair-related endpoint because no such study has ever been conducted.
Yes — must continue indefinitely
Unknown for hair. No study has examined what happens when BPC-157 is stopped in any context related to hair or scalp health.
Side effects, contraindications, and special populations
| Adverse event | Rate | Placebo | Notes |
|---|---|---|---|
| Injection site reactions (if injected) | Unknown — no controlled trial data; commonly reported anecdotally | — | Redness, soreness, and mild swelling at the subcutaneous injection site are the most frequently reported side effects in self-experimentation communities. These are typical of any subcutaneous peptide injection and not unique to BPC-157. |
| Nausea / GI discomfort | Unknown — reported anecdotally, especially at higher doses | — | Mild nausea and stomach upset are commonly reported in self-experimentation communities, particularly during the first few days of use. This is ironic given BPC-157's gastroprotective properties in animal models, but no controlled human data exists to quantify the rate. |
| Dizziness / lightheadedness | Unknown — reported anecdotally | — | Commonly reported in self-experimentation forums, typically mild and transient. May be related to BPC-157's nitric oxide modulation and potential vasodilatory effects. No formal incidence data exists. |
| Headache | Unknown — reported anecdotally | — | Mild headaches reported by some users, especially when initiating use. Could be related to angiogenic or vasodilatory activity. No controlled data to establish causality. |
| Fatigue / lethargy | Unknown — reported anecdotally | — | Some users report transient fatigue. No scientific basis to determine whether this is a true pharmacological effect or coincidental. |
- Theoretical tumor promotion via angiogenesis (Unknown — theoretical risk, not documented in preclinical or limited human data) — BPC-157 upregulates VEGFR2 and promotes new blood vessel formation. Angiogenesis is a hallmark of tumor growth and metastatic progression. Any compound that promotes neovascularization could theoretically facilitate tumor expansion. No tumor-promoting effects have been documented in BPC-157 studies to date, but these studies were not designed to detect long-term oncologic outcomes, and the total human exposure is far too small to assess cancer risk.
- Immunogenicity (peptide-specific risk) (Unknown — identified as a concern by the FDA but not studied) — The FDA's Category 2 classification specifically cited immunogenicity as a safety concern for BPC-157 in compounding. As a synthetic peptide, BPC-157 could trigger immune responses including antibody formation. No immunogenicity studies have been published in humans.
- Product contamination and purity (supply chain risk) (Unknown but potentially significant) — Since BPC-157 has no regulatory approval, products sold online are unregulated. USADA and the FDA have warned that peptide products from unregulated sources may contain impurities, incorrect doses, or contaminating substances. There is no USP monograph or pharmacopeial standard for BPC-157. Users purchasing from research chemical suppliers or overseas vendors have no assurance of purity or identity.
- Unknown long-term effects (Completely unknown) — The longest published human exposure is the Phase II UC trial (duration not publicly disclosed) and a few-week IV pilot in 2 subjects. No long-term safety data exists in humans. The effects of chronic BPC-157 use over months or years — as many self-experimenters practice — are entirely unknown.
- Active malignancy or high cancer risk (Theoretical but serious) — BPC-157's pro-angiogenic mechanism (VEGFR2 upregulation) could theoretically promote tumor vascularization and growth. Patients with active cancer, a history of cancer, or significant cancer risk factors should avoid BPC-157. No clinical data exists to quantify this risk, but the biological plausibility is strong.
- Pregnancy and lactation (Absolute contraindication (no data)) — No human reproductive safety data exists. While preclinical studies in animals showed no embryo-fetal toxicity (Xu et al., 2020), this does not guarantee safety in humans. BPC-157's angiogenic and growth-factor-modulating properties make it a theoretical concern during fetal development.
- Bleeding disorders or anticoagulant therapy (Theoretical) — BPC-157 modulates nitric oxide synthesis and promotes angiogenesis, both of which can affect hemostasis. Patients with bleeding disorders or on anticoagulant therapy may require careful evaluation. No clinical data exists on this interaction.
- WADA-tested athletes (Absolute — banned substance) — BPC-157 has been on the WADA Prohibited List since 2022 under category S0 (Unapproved Substances). Athletes under WADA jurisdiction face sanctions if detected. No Therapeutic Use Exemption (TUE) can be granted because BPC-157 is not an approved therapeutic agent.
- Nitric oxide pathway medications (nitrates, PDE5 inhibitors like sildenafil/tadalafil) (Theoretical) — BPC-157's bidirectional modulation of the nitric oxide system creates theoretical interaction potential. Concurrent use with nitrates or PDE5 inhibitors could theoretically potentiate hypotensive effects. No adverse interactions documented in published literature, but no formal drug interaction studies exist.
- Anti-angiogenic therapies (bevacizumab, sunitinib, etc.) (Theoretical — mechanistic antagonism) — BPC-157 promotes angiogenesis via VEGFR2 upregulation. Anti-angiogenic cancer therapies work by blocking VEGF signaling. Concurrent use would be mechanistically contradictory and could undermine cancer treatment efficacy. This is a strong theoretical contraindication.
- Dopaminergic medications (Theoretical) — BPC-157 interacts with the dopamine system in preclinical models (attenuates amphetamine effects, blocks haloperidol supersensitivity). Theoretical interaction with dopamine agonists, antagonists, or L-DOPA. No human data exists.
- Cardiovascular medications (antihypertensives, vasodilators) (Theoretical) — BPC-157's NO modulation and angiogenic activity could theoretically interact with blood pressure medications. No documented interactions, but no formal studies have been conducted.
Absolutely contraindicated due to complete absence of human reproductive safety data. Preclinical animal studies (mice, rats, rabbits) showed no embryo-fetal toxicity, but this is insufficient to establish human safety. BPC-157's angiogenic and growth-factor-modulating properties present theoretical risks to fetal development.
No sex-specific safety data exists. All published human studies included small mixed-sex cohorts or did not report sex-stratified safety data. Women of childbearing potential should use contraception if using BPC-157, though the compound is not approved for any use.
Absolutely contraindicated. No pediatric safety or efficacy data exists for any indication. The effects of exogenous angiogenic peptides on developing tissues are unknown and potentially concerning.
Every claim, traced back to its source
We took every major claim made about BPC-157 and matched it to the specific experimental model behind it. Click a claim to see the model, the finding, and our assessment of how much weight it deserves.
8 claims · evidence-by-evidence breakdown
1In SilicoWeight: Very LowBPC-157 promotes hair growth through improved blood flow to folliclesPure extrapolation from tissue repair studies — zero direct evidence for hair growth in any model.
No model — this claim has zero published, peer-reviewed evidence. No study on PubMed has tested BPC-157 on hair follicles, hair cycling, or hair growth as a primary endpoint. The claim is entirely extrapolated from BPC-157's proven pro-angiogenic (blood-vessel-forming) activity in wound healing models.
There is no finding to report. No researcher has published data showing BPC-157 stimulates hair growth in any model — not in cell culture, not in mice, not in humans. The theoretical link is: BPC-157 upregulates VEGFR2 (a blood vessel growth receptor) → more blood vessels → better follicle nutrition. But this chain of logic has never been tested in hair tissue.
This is pure extrapolation. VEGF-mediated angiogenesis is a real mechanism (it's part of how minoxidil works), but "increases blood flow in a rat hind limb" does not mean "regrows hair on your scalp." BPC-157 has no demonstrated connection to any hair-specific pathway: no Wnt/β-catenin signaling, no DHT modulation, no follicle stem cell activation, no dermal papilla cell data. If someone is selling you BPC-157 specifically for hair regrowth, they are extrapolating from tissue repair studies that never examined hair.
- N/A (2026). No peer-reviewed studies exist for BPC-157 and hair growth
2In SilicoWeight: Very LowBPC-157 addresses the pathways that drive androgenetic alopeciaBPC-157's mechanism of action has zero overlap with the pathways that drive pattern hair loss.
No model. This claim is false based on current published evidence.
BPC-157's demonstrated mechanisms — VEGFR2-mediated angiogenesis, nitric oxide synthesis, anti-inflammatory cytokine modulation — do not address DHT (the primary driver of androgenetic alopecia), follicle miniaturization, or Wnt/β-catenin signaling (the pathway that tells follicles to enter anagen). More blood flow to a miniaturizing follicle doesn't reverse the miniaturization.
BPC-157 may be a great peptide for other applications, but its mechanism of action has no overlap with the pathways that drive pattern hair loss. This is the central problem: you can have a potent, well-studied compound that simply doesn't target the right biology. As the evidence stands, BPC-157 for hair loss is a category error.
- N/A (2026). The claim itself is unsupported — no studies link BPC-157 to AGA pathways
3In VivoWeight: Moderate-HighBPC-157 protects the gut lining and heals ulcersBest-supported use case — extensive preclinical data, but the only human trial was never fully published.
In vivo — Wistar rats. Multiple ulcer models tested: restraint stress (48 hours), subcutaneous cysteamine, intragastric 96% ethanol, colitis, ischemia/reperfusion, colocutaneous fistulas, and ileoileal anastomosis. This is BPC-157's most extensively studied domain — dozens of rat studies spanning 30+ years.
BPC-157 consistently showed gastroprotection across all ulcer models. In colitis models, it reduced inflammation and promoted mucosal healing. In fistula models, it accelerated closure. In anastomosis models, it promoted intestinal healing. A Phase II clinical trial for mild-to-moderate ulcerative colitis (PL14736, conducted by Pliva pharmaceutical in Croatia) was described as "effective with no toxicity" — but the full data from this trial has never been published in a standalone peer-reviewed paper.
The gut healing data is the strongest in BPC-157's portfolio. Multiple models, consistent results over decades, and biological plausibility (BPC-157 is derived from gastric juice protein). The major limitation is that the Phase II human trial results were never fully published — they're referenced only in passing in other Sikiric review articles. Without seeing the actual data (endpoints, effect sizes, adverse events), you can't evaluate the human evidence. No Phase III trial was ever conducted.
- Sikiric et al. (1993). Original characterization of BPC-157 PMID 8298609
- Sikiric et al. (1994). Gastroprotection studies PMID 7904712
- Sikiric et al. (2012). Ulcerative colitis review PMID 22300085
- Klicek et al. (2008). Fistula healing PMID 18818478
- Duzel et al. (2017). Colitis model PMID 29358856
4In VivoWeight: Moderate-HighBPC-157 accelerates tendon and ligament healingSecond-strongest use case — independently replicated mechanism, but zero human trials for this indication.
In vivo — rats (Achilles tendon transection, MCL ligament transection). Also in vitro — rat tendon fibroblasts and tendon explant outgrowth assays. Importantly, two key mechanistic studies (FAK-paxillin pathway, growth hormone receptor upregulation) were independently replicated by Chang Gung University in Taiwan — not from the Zagreb group.
BPC-157 improved Achilles tendon healing biomechanically (increased load of failure), functionally (higher Achilles Functional Index), and microscopically (better collagen organization). MCL healing improved over 90 days regardless of administration route (IP, oral, or topical cream). Mechanistically, BPC-157 activates the FAK-paxillin pathway for cell migration and upregulates growth hormone receptor expression in tendon fibroblasts.
This is probably BPC-157's second-strongest evidence area after gut healing. The independent replication from Taiwan is significant — it means the FAK-paxillin mechanism isn't just one lab's finding. The 90-day MCL study showing effectiveness across multiple routes of administration is also compelling. However, there are zero human trials for tendon/ligament healing with BPC-157. A 2025 systematic review (Vasireddi et al., PMID 40756949) found 36 studies on BPC-157 for musculoskeletal healing: 35 were preclinical, 1 was a small retrospective chart review.
- Staresinic et al. (2003). Achilles tendon healing PMID 14554208
- Chang et al. (2011). FAK-paxillin pathway (independent replication) PMID 21030672
- Chang et al. (2014). Growth hormone receptor upregulation (independent replication) PMID 25415472
- Cerovecki et al. (2010). MCL ligament healing PMID 20225319
5In VivoWeight: Moderate-HighBPC-157 promotes blood vessel formation through VEGFR2 activationKey mechanistic paper with independent replication — but angiogenesis alone does not address hair loss biology.
In vitro — human vascular endothelial cells (HUVECs). In vivo — chick chorioallantoic membrane (CAM) assay and rat hind limb ischemia model. This is the key mechanistic paper (Hsieh et al., 2017), independently conducted at Chang Gung University/Taipei Medical University in Taiwan.
BPC-157 increased VEGFR2 expression (but not VEGF-A itself) in human endothelial cells, promoted VEGFR2 internalization, and activated the VEGFR2-Akt-eNOS signaling cascade. In the CAM assay, it increased vessel density. In ischemic rat limbs, it accelerated blood flow recovery.
This is the single most important paper for understanding how BPC-157 works. The mechanism is clear and specific: BPC-157 upregulates the VEGF receptor (not the ligand), promoting angiogenesis. The independent replication from Taiwan gives this extra credibility. However, the clinical relevance depends entirely on the application — angiogenesis matters for wound healing and ischemic tissue, but as discussed above, it doesn't address the mechanisms driving hair loss.
- Hsieh et al. (2017). VEGFR2 activation and angiogenesis PMID 27847966
- Hsieh et al. (2020). Src-Cav1-eNOS signaling pathway PMID 33051481
6In VivoWeight: ModerateBPC-157 accelerates muscle healing after injuryConsistent rat data for muscle repair, but single-lab and no human trials.
In vivo — rats (quadriceps crush injury model, force 0.727 Ns/cm²). Routes tested: intraperitoneal or local cream application, immediately after injury.
BPC-157 improved muscle healing across all measured parameters: macroscopic (less hematoma, edema, no leg contracture), microscopic (better tissue organization), functional (improved movement), and biochemical (reduced creatine kinase, LDH, AST, ALT — all markers of muscle damage). A separate study showed it also counteracted corticosteroid-induced impairment of muscle healing.
Consistent animal data showing real muscle repair benefits, but these are all rat studies from the Zagreb group. No human trial has ever tested BPC-157 for muscle healing. The corticosteroid interaction data is interesting clinically, since many patients deal with steroid-impaired healing, but it hasn't been validated in humans.
- Novinscak et al. (2008). Muscle healing after crush injury PMID 18668315
- Sikiric et al. (2010). Counteracting corticosteroid-impaired muscle healing PMID 20190676
7In VivoWeight: ModerateBPC-157 has neuroprotective effects and interacts with the dopamine systemIntriguing neuroprotection data across multiple models, but entirely preclinical and far from clinical application.
In vivo — rats and mice. Models include: amphetamine-induced stereotypy, sciatic nerve transection, spinal cord compression injury, and traumatic brain injury (TBI by falling weight). Administration routes varied (IP, intragastric, local).
In the dopamine studies, BPC-157 attenuated amphetamine-induced stereotypic behavior and blocked haloperidol-induced supersensitivity. In nerve injury, it promoted faster axonal regeneration with increased density of myelinated fibers and thicker myelin sheaths. After spinal cord injury, a single IP injection produced significantly higher motor scores and less grey matter damage. After TBI, it reduced brain damage and improved early outcomes.
The neuroprotection data is intriguing but all preclinical. The dopamine system interaction is particularly interesting because it suggests BPC-157 could have applications beyond simple tissue repair — potentially in neurodegenerative or psychiatric contexts. But these are animal models, and the distance from "reduced stereotypy in amphetamine-treated rats" to any human neurological treatment is enormous.
- Jelovac et al. (1998). Dopamine system interaction PMID 9547930
- Gjurasin et al. (2010). Sciatic nerve regeneration PMID 19903499
- Perovic et al. (2019). Spinal cord injury PMID 31266512
- Comprehensive review (2022). Neural regeneration review. Neural Regen Res PMID 34380875
8Open-LabelWeight: Moderate-HighBPC-157 is extremely safe with no known toxic doseExceptional preclinical safety (no LD50 in any species), but total human data covers only ~75 subjects.
Preclinical toxicology — mice, rats, rabbits, and dogs, at doses from 6 µg/kg to 20 mg/kg across multiple routes (IM, IP, IV, oral). Also limited human data: a Phase II UC trial (unpublished details), a 2-person IV safety pilot, a 17-patient knee injection retrospective, and a 12-patient interstitial cystitis pilot.
No LD50 has ever been established — meaning researchers could not find a lethal dose in any species. No acute toxicity, no organ damage (liver, kidney, brain, etc.), no genetic toxicity, no embryo-fetal toxicity. In the limited human data, no serious adverse events were reported across approximately 75 total subjects.
The preclinical safety profile is genuinely remarkable — it's rare for a compound to have no identifiable toxic dose across four species. However, the total human exposure is extremely small (~75 subjects across all trials, most in very small studies). The IV safety pilot tested only 2 people. The Phase II UC trial never published full safety data. Also critical: all three US-based human studies were conducted by the same author (Lee E.) and published in the same low-impact CAM journal. More independent human safety data is needed before drawing firm conclusions.
- Xu et al. (2020). Preclinical toxicology review PMID 32334036
- Lee et al. (2021). Knee injection retrospective PMID 34324435
- Lee et al. (2024). Interstitial cystitis pilot PMID 39325560
- Lee & Burgess (2025). IV safety pilot PMID 40131143
What's still missing from the science
- Any study — in any model — testing BPC-157 on hair follicles, hair cycling, or hair growth.
- Any connection to DHT, Wnt/β-catenin, or follicle miniaturization pathways.
- A fully published, peer-reviewed Phase II or Phase III human clinical trial for any indication. The UC trial data remains proprietary.
- Significant independent replication. Most claims rest on one lab's work (Zagreb). The Taiwan group has replicated the VEGFR2 and FAK-paxillin mechanisms, but most other findings lack independent confirmation.
- A published human trial with more than 20 subjects for any indication (excluding the Phase I safety study in healthy volunteers).
Our verdict on BPC-157
Not in our formulary yet
We don't carry this ingredient. We only formulate around actives where the evidence — and the safety profile — is strong enough to recommend with confidence. As the data matures, we may revisit.
From the Anagen blog
Long-form analysis and primary-source breakdowns that go beyond the summary above.
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