No human dose established
All dosage figures on this page are from rodent preclinical studies. No clinical trial has established a therapeutic human dose for BPC-157, TB-500, or GHK-Cu, individually or in combination. Rodent dose figures do not translate directly to human dosing.
Fig. 07 / Research dosing timeline
Tissue changes accruing over days in rodent studies — from the first dose bud to full healing at the vine's end.
BPC-157 Research Dosing Ranges
| Dose | Route | Model | Outcome | Ref |
|---|---|---|---|---|
10 μg/kg/day |
Intraperitoneal | Rat Achilles tendon transection | Improved AFI scores, biomechanical properties, reduced inflammation | [4] |
10 μg/kg and 10 ng/kg |
IP, oral, topical | Rat medial collateral ligament | Consistent healing improvements over 90-day study period | [8] |
10 μg/kg and 10 ng/kg |
IP and oral | Rat NSAID liver injury model | Normalized liver enzymes, prevented encephalopathy | [5] |
20–500 μg/kg |
IM and IV | PK study — rat and beagle dog | t½ ~15.2 min (rat IV), ~5.27 min (dog IV); IM bioavailability 14–51% | [7] |
10 μg/kg |
Oral (drinking water) | Rat IBD/mucosal models | Anti-ulcer, mucosal healing, cytoprotective activity | [22] |
BPC-157 dosage in rodent studies spans a remarkably wide range depending on model and route. Tissue-repair and healing studies most commonly use 10 μg/kg/day intraperitoneally. Ultra-low-dose studies confirm efficacy at 10 ng/kg.[5][8] The literature documents efficacy across a wide range, suggesting a flat or plateau dose-response curve rather than a strict threshold effect in rodent models.
The BPC-157 dosage in research literature does not establish a human clinical dose. No dose-ranging study in humans has been published. The three published human pilot studies did not report a standardized dose schedule.[21]
TB-500 dose ranges in wound healing models span 0.5–10 mg/kg.[22] No TB-500-fragment-specific human pharmacokinetic study has been published.
BPC-157 TB-500 Blend Dosage Protocols in the Literature
The BPC-157 TB-500 blend dosage most commonly referenced in research-community literature uses equal proportioning of the two components: 5 mg:5 mg or 10 mg:10 mg per vial.[22] These formulations are conventions built on individual compound dose ranges, not controlled combination trials. BPC-157 rodent studies use 10 μg/kg (IP) as the primary tissue-repair dose; TB-500 rodent wound healing studies use 0.5–10 mg/kg — a much wider range reflecting variation across wound models and species.[4][22] The orders-of-magnitude difference in individual-compound rodent dose ranges means that designing a rationally grounded 1:1 blend is not straightforward from the literature alone; the 5:5 convention is a practical research-community compromise, not an evidence-based fixed ratio.
BPC-157 Pharmacokinetics and Bioavailability
BPC-157 pharmacokinetics in rats show an intravenous elimination half-life of approximately 15.2 minutes and intramuscular bioavailability of 14–19%. In beagle dogs, IV half-life is approximately 5.27 minutes with IM bioavailability of 45–51%.[7] The compound is excreted primarily via urine and bile with linear pharmacokinetic characteristics.
BPC-157 is stable in gastric juice for more than 24 hours — a property that provides the mechanistic basis for the observed oral-route systemic effects in rodent studies.[7] In oral drinking-water models (10 μg/kg in 12 mL per rat per day), BPC-157 demonstrated anti-ulcer, mucosal healing, and cytoprotective activity consistent with systemic absorption.[22]
Administration Routes Studied in BPC-157 Research
BPC-157 has been studied via: intraperitoneal injection, subcutaneous injection, intramuscular injection, intravenous injection, oral gavage, oral drinking water, and topical cream application.[4][7][8][22] Consistent healing effects were documented via all three primary routes (intraperitoneal, topical, oral) in the medial collateral ligament study over a 90-day period[8] — a notable finding suggesting the compound is active regardless of route in rodent tissue-repair models. TB-500 has been studied topically, intraperitoneally, and subcutaneously.[10][11] GHK-Cu has been studied topically, intradermally, systemically in animal models, and in liposomal topical formulations.[14][17]
Injection Frequency in BPC-157 TB-500 Research Protocols
Rodent studies typically administer BPC-157 once daily subcutaneously or intraperitoneally — the Krivic 2006 tendon model used daily IP injection over the study period;[4] the Cerovecki 2010 ligament study used daily IP and oral administration over 90 days.[8] TB-500 administration in studies ranges from daily to twice-weekly depending on the injury model and observation period. No consensus human protocol exists in the peer-reviewed literature for either compound, individually or in combination.
Reconstitution of BPC-157 TB-500 Blend: Laboratory Protocols
Research-grade peptide vials are lyophilized (freeze-dried) for stability. Published research protocols describe reconstitution with bacteriostatic water (0.9% benzyl alcohol saline) at concentrations of 1–2 mg/mL.[24] GHK-Cu solution exhibits a characteristic blue-green color upon reconstitution due to copper(II) chelation — an expected chemical property of copper(II) complexes, not an indicator of degradation.[24] Lyophilized peptide blends are typically stored at −20°C long-term and 2–8°C after reconstitution. BPC-157 and TB-500 rodent studies most commonly use subcutaneous or intraperitoneal injection routes.
Timeline: When Do BPC-157 and TB-500 Show Effects in Studies?
In rat tendon and muscle models, measurable tissue changes with BPC-157 appear within 7–14 days of dosing — the Krivic 2006 tendon study documented improved AFI scores and biomechanical properties; the Cerovecki 2010 ligament study showed improvements at multiple time-points across 90 days.[4][8] Thymosin beta-4 wound healing studies in rats show reepithelialization changes within 4–7 days.[10] GHK-Cu liposomal wound healing shortened time to closure to 14 days in the mouse scald model.[17] No validated human timeline exists.
GHK-Cu Studied Concentrations
GHK-Cu is active in fibroblast culture at 10⁻¹² to 10⁻⁹ M — concentrations in the picomolar-to-nanomolar range.[16] Plasma endogenous GHK levels are approximately 200 ng/mL at age 20 and approximately 80 ng/mL by age 60 — providing a natural reference point for the molecule's physiological concentration range.[14] No injectable synthetic GHK-Cu pharmacokinetic study has been identified in the published literature; topical formulation strategies (palmitoylation, copper complexation, liposomal encapsulation) are the primary delivery research focus.[26]