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TB-5007 residuesLKKTETQEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: TB-500, TB500, Ac-LKKTETQ
Reepithelialization up 42% at day 4 and 61% at day 7 in preclinical wound models (Malinda et al.)[1]. TB-500 is a synthetic 7-amino acid fragment (Ac-LKKTETQ) of the 43-amino acid thymosin beta-4 protein. It promotes angiogenesis, reduces fibrosis, and accelerates cell migration to injury sites. The fragment itself has never completed a human clinical trial; the only Phase I data [2] tested the full parent protein. Community evidence across 500+ Reddit threads tells a different story: consistent reports of tendon, ligament, and muscle recovery within 3 to 4 weeks of loading. One catch: TB-500 was removed from FDA Category 2 on April 15, 2026. Compounding pharmacy access awaits PCAC review starting July 2026.
Seven amino acids. That is all TB-500 is. Acetylated leucine-lysine-lysine-threonine-glutamate-threonine-glutamine, pulled from positions 17 through 23 of the 43-amino-acid thymosin beta-4 protein. CAS number 885340-08-9, molecular weight 846.97 Da. The mechanism is well characterized in animals. TB-500 binds monomeric G-actin, sequestering free actin subunits and remodeling the cytoskeleton so that endothelial and immune cells migrate faster to damaged tissue. It upregulates VEGF 2.5 to 3.8-fold. Malinda and colleagues confirmed that thymosin beta-4 increased reepithelialization by 42% at day 4 and 61% at day 7 versus controls in corneal wound models [1]. It also suppresses myofibroblast differentiation, which reduces scar formation. What makes TB-500 unusual is systemic distribution. You don't need to inject near the injury. Subcutaneous injection in the abdomen reaches a torn rotator cuff the same way it reaches a strained hamstring. Community users have validated this property thousands of times over. The first fragment-specific human trial (NCT07487363) began recruiting in 2026 for an ASCVD indication with approximately 80 subjects. No results are available yet. A 2024 metabolite study by Rahaman and colleagues added a wrinkle: the parent compound showed no wound-healing activity in vitro. The metabolite Ac-LKKTE was the active species. That finding has not changed community dosing practices, but it raises questions about mechanism attribution. Community confidence (4.1/5 sentiment, 500+ r/Peptides threads) sits well ahead of the formal evidence base. TB-500 was on the FDA Category 2 list from 2024 until April 15, 2026, when HHS removed it. Compounding pharmacy access awaits PCAC review starting July 2026. All current supply comes from unregulated gray-market vendors.
TB-500 works through actin dynamics. The peptide binds to monomeric G-actin and sequesters free actin subunits, shifting the balance of cytoskeletal assembly inside cells. When cells need to migrate to an injury site, they depend on rapid actin polymerization at the leading edge. TB-500 regulates that process. This actin-sequestering activity drives two downstream effects. The first is angiogenesis. TB-500 upregulates vascular endothelial growth factor (VEGF) 2.5 to 3.8-fold in preclinical models. More capillaries at the injury site mean better oxygen delivery and faster tissue remodeling. The second downstream effect is anti-fibrotic. TB-500 inhibits myofibroblast differentiation, the process responsible for excessive scar tissue formation. In preclinical wound models, this translated to cleaner healing with less fibrosis. Malinda and colleagues published the foundational wound healing data in 1999 [1]. Thymosin beta-4 increased reepithelialization by 42% at day 4 and 61% at day 7 versus controls. Bock-Marquette and colleagues confirmed cardioprotective effects after myocardial infarction in animal models [3]. A 2026 review in Cureus (PMC12753158) placed TB-500 among the most promising orthopedic peptides based on preclinical data quality. One important caveat: a 2024 metabolite study found that the TB-500 parent compound had no wound-healing activity in vitro. The metabolite Ac-LKKTE was the active species. In-vivo activity may depend on metabolic conversion.
Strong preclinical evidence for thymosin beta-4 and its active fragment in wound healing, angiogenesis (VEGF upregulation 2.5–3.8×), and actin-mediated cell migration. Fragment-specific human data is nearly absent: the only published Phase I human trial [2] used full 43-AA thymosin beta-4, not the 7-AA TB-500 fragment. A 2024 metabolite study (Rahaman et al., J Chromatogr B) found the TB-500 parent compound had no wound-healing activity in vitro: metabolite Ac-LKKTE was the active species, introducing uncertainty about in vivo mechanism attribution. First fragment-specific human trial (NCT07487363, ASCVD indication, ~80 subjects) recruiting as of April 2026: no results yet.
Malinda et al. 1999, "Thymosin beta 4 accelerates wound healing," J Invest Dermatol. PMID 10469335: full TB4 increased reepithelialization 42% at day 4 and 61% at day 7 vs. controls in preclinical corneal wound models; foundational study establishing the wound healing mechanistic basis (note: tested full TB4, not TB-500 fragment)
No completed Phase II/III human trial for the TB-500 fragment specifically. The only published human Phase I (PMID 34346165) tested full 43-AA thymosin beta-4: PK and safety data cannot be directly applied to the 7-AA fragment. 2024 metabolite study suggests the parent peptide may be inactive in vitro; in-vivo activity may depend on metabolic conversion to Ac-LKKTE. No published human PK characterization for TB-500 fragment. Long-term safety unknown. Theoretical oncogenic risk from pro-angiogenic mechanism is unresolved. No rodent-validated human dose range.
One of the most trusted healing peptides in the research community (4.1/5 sentiment, 500+ r/Peptides threads). Standard loading/maintenance structure is well-established and consistently reproduced across community reports. Most valued for tendon, ligament, and muscle injury recovery. Key advantage repeatedly cited: systemic action means no need to inject at the injury site. Main concerns are cost and sourcing quality variability under current FDA restrictions.
Community protocols are consistent with the preclinical mechanistic data (angiogenesis, actin sequestration, systemic distribution). However, the 2024 metabolite study challenges direct attribution of wound-healing activity to the parent peptide, and no human RCT for the fragment exists. Community confidence significantly exceeds what the fragment-specific evidence base strictly supports. The systemic dosing approach (injection site irrelevance) is mechanistically well-grounded.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 2mg | 2x/week |
| Moderate | 2,500mcg | 2x/week |
| Aggressive | 5mg | 2x/week |
All TB-500 dosing is community-driven. No human dose-finding study exists for the fragment. Beginner: 2000 mcg (2 mg) twice weekly. Moderate: 5000 mcg (5 mg) twice weekly. Aggressive: 7500 mcg (7.5 mg) twice weekly. Reconstitution math for a 5 mg vial with 1 mL bacteriostatic water: concentration is 5000 mcg per mL. Each 10 units on a 100-unit insulin syringe equals 500 mcg. So 2000 mcg (beginner dose) is 40 units. For a 10 mg vial with 1 mL BAC water: 10,000 mcg per mL, meaning 20 units for 2000 mcg. The loading phase matters more than anything else. Skipping it is the single most common reason for disappointing results. You need 2 injections per week for at least 4 to 6 weeks to build adequate tissue-level concentrations. Going straight to once-weekly maintenance is an underdose. Don't train through the injury during a TB-500 protocol. The community figured this out quickly: TB-500 accelerates repair, but it doesn't protect against re-injury from continued loading of the damaged tissue. Relative rest of the injured structure speeds outcomes. Injection site does not need to be near the injury. Abdomen or thigh, alternating sides.
Loading phase: full dose 2x/week for 4-6 weeks. Then maintenance: half dose 1x/week. Repeat loading if needed for new injuries.
No published safety data exists for TB-500 use beyond 12 continuous weeks in humans. Cycling (6 weeks on / 2 weeks off as a short cycle, or 12 weeks on / 4–6 weeks off for full protocols) is a community-driven precaution in the absence of long-term human safety evidence. The pro-angiogenic mechanism does not carry a well-characterized receptor desensitization risk, so cycling is primarily about limiting cumulative exposure to an understudied compound rather than managing downregulation.
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Expected: Noticeable pain reduction and improved range of motion by weeks 3–4; significant soft tissue improvement by end of loading phase; full healing of moderate injuries possible by week 12
Monitor: Monitor for injection site reactions, fatigue, and headache during loading phase. These are common and typically self-resolve by week 3. Fever above 100.4°F or skin rash requires stopping and medical evaluation.
Aim the stream against the glass wall, not directly onto the powder. Swirl gently until dissolved. Concentration: 5000 mcg per mL.
Beginner (2000 mcg): draw to the 40-unit mark. Moderate (5000 mcg): draw to the 100-unit mark (full syringe). For a 10 mg vial reconstituted with 1 mL BAC water (10,000 mcg/mL), beginner dose is 20 units.
Pinch a fold of skin on the abdomen or thigh. Insert a 27 to 29 gauge, 0.5 inch needle at a 45-degree angle. Push the plunger slowly.
Abdomen left, abdomen right, thigh left, thigh right. Injection site does not need to be near the injury; TB-500 distributes systemically.
No fasting requirement. Space injections 3 to 4 days apart during loading (e.g., Monday and Thursday).
Maintenance phase: 1 injection per week. Reload at full loading dose and frequency if a new injury occurs.
Storage after reconstitution: refrigerate at 2 to 8 degrees C (36 to 46 degrees F). Use within 3 to 4 weeks. Lyophilized (unreconstituted) vials are stable refrigerated for up to 24 months.
"Wolverine Stack": the dominant pairing in the community. BPC-157 provides targeted local healing (inject near injury site); TB-500 provides systemic angiogenesis and anti-fibrotic effect. Community widely considers this the most effective healing combination available. Both are WADA prohibited.
BPC-157 250–500 mcg near injury site 1–2×/day + TB-500 2 mg 2×/week systemically; run concurrently throughout loading phase
GH pulse support for anabolic recovery and improved sleep during healing. Community rationale: TB-500 accelerates tissue repair; ipamorelin provides GH axis support to maximize protein synthesis and recovery quality.
100–200 mcg ipamorelin pre-sleep alongside standard TB-500 protocol
Paired with ipamorelin to amplify GH pulse for recovery support. Common in intermediate and advanced healing stacks; provides GHRH + GHRP synergy.
100 mcg CJC-1295 no-DAC + 100 mcg ipamorelin pre-sleep
Added to TB-500 protocols targeting skin wound healing or post-surgical recovery. GHK-Cu provides collagen stimulation and gene-level repair activation; TB-500 provides systemic angiogenesis. Community reports this combination for wound and skin healing.
TB-500 upregulates VEGF 2.5–3.8-fold. Anti-VEGF agents directly antagonize this mechanism. Concurrent use creates direct pharmacodynamic opposition and defeats the purpose of TB-500.
Do not combineChronic high-dose NSAIDs may blunt TB-500 angiogenic signaling through prostaglandin pathway suppression. Noted in tb500.json extraction. Short-term/low-dose NSAID use for acute pain management is unlikely to be clinically significant.
TB-500 promotes angiogenesis at healing sites. Concurrent anticoagulation may increase bleeding risk at sites of active new vascular formation.
TB-500 modulates immune cell migration and angiogenic pathways. Effect of combining with systemic immunosuppression is unknown; potential for altered immune regulation.
Pricing updated 2026-04-09
TB-500 has never completed a Phase II or Phase III human trial. The only published Phase I [2] tested full 43-amino-acid thymosin beta-4 in 36 healthy Chinese volunteers, not the 7-amino-acid TB-500 fragment. Safety data for the fragment comes almost entirely from community self-reports. Injection site reactions are the most frequently reported problem. Redness, swelling, and tenderness at the injection site appear in a large percentage of users. Rotating between abdomen and thigh reduces local accumulation. Blistering, progressive swelling, or spreading warmth beyond the injection site is abnormal and requires stopping immediately. Fatigue and lethargy during the loading phase (weeks 1 to 2) rank second. Community reports describe this as the most common early side effect at doses of 4 to 5 mg per week. It usually resolves by week 3 without dose adjustment. If fatigue is debilitating, stepping down to 2 mg twice weekly is the standard community recommendation. Headache during loading is common and typically follows the same resolution pattern as fatigue. Nausea is less frequent. Rare but serious reactions include fever above 100.4 degrees F, injection site blistering, skin rash, hives, and muscle aches. Any of these require stopping the protocol and seeking medical evaluation. The unresolved long-term concern is oncogenic risk. TB-500 is pro-angiogenic. It promotes new blood vessel formation. In the presence of occult tumor tissue, this mechanism could theoretically support vascularization and tumor growth. Active cancer or personal cancer history is an absolute contraindication at any dose. Baseline age-appropriate cancer screening (PSA, mammogram, colonoscopy as applicable) is recommended before starting, particularly for anyone over 40. TB-500 is WADA prohibited (S2: Growth Factors) in and out of competition. A 4-year ban was issued in 2024 for documented use. DoD personnel face the same restriction. Pregnancy and breastfeeding: no safety data exists. Do not use.
Verify TB-500 dosing and safety with a second opinion
TB-500 was an FDA Category 2 bulk drug substance from 2024 to April 15, 2026, when HHS removed it. Compounding by 503A/503B pharmacies is not yet available (PCAC review pending). All current US market supply comes from unregulated gray-market research vendors. Endotoxin contamination, mislabeling, and significant underdosing are documented community concerns. No pharmaceutical-grade compounding source is currently legally available.
| Test | When | Target |
|---|---|---|
| Baseline cancer screening | Before starting, especially for anyone over 40 or with family history of cancer | Age-appropriate cancer screening current (PSA, mammogram, colonoscopy as applicable); no active malignancy |
| CBC and CMP (comprehensive metabolic panel) | Baseline before starting; optional recheck at 6–8 weeks for longer protocols | — |
| Injection site self-assessment | Each injection: visual inspection and palpation before and after | Minor transient redness and mild tenderness are expected and normal; spreading, progressive, or blistering reactions are abnormal and require stopping |
TB-500 is pro-angiogenic: it promotes new blood vessel formation. In the presence of occult or undiagnosed tumor tissue, this mechanism could theoretically support vascularization and tumor growth. Active or historical cancer is an absolute contraindication.
No specific TB-500 safety biomarkers exist. CBC/CMP as general health baseline to detect subclinical conditions that would be contraindications (active infection, hepatic/renal impairment).
Early detection of infection (spreading redness, warmth, induration beyond expected local reaction) or allergic response (hives, blistering, spreading rash)
Loading phase begins: 2x/week at full dose. Mild systemic effects may include temporary lethargy or headache. Inflammation reduction may begin within days.
Loading phase continues. Noticeable improvement in pain levels, flexibility, and range of motion around injured areas. New blood vessel formation (angiogenesis) accelerates tissue repair.
End of loading phase. Significant healing progress in soft tissue injuries. Many users report substantially reduced pain and improved function.
Transition to maintenance: half dose, 1x/week. Continued healing support. Reload at full dose if a new injury occurs.
Weeks 1 to 2: Loading begins at full dose twice weekly. Angiogenic signaling kicks in at the cellular level, with VEGF upregulation and actin sequestration starting to draw immune and endothelial cells toward injury sites. You won't feel much improvement in the injury itself yet. Fatigue, mild headache, and injection site tenderness are the most common early complaints. Weeks 3 to 4: This is usually when TB-500 starts to prove itself. Most users describe noticeable improvement in pain levels, flexibility, and range of motion. Tendon and ligament injuries tend to show the clearest early response. Loading phase side effects typically fade by week 3. Weeks 5 to 6: Peak loading effect. Accumulated angiogenesis and tissue remodeling from the loading phase produce the most visible healing progress. Fibrosis suppression contributes to better tissue quality and less scar formation. Many users report near-full functional return by the end of loading. Weeks 7 to 12: Transition to maintenance at half dose, once weekly. Continued gradual improvement for complex injuries. Some users stop at week 8 if the injury is resolved; others carry maintenance to week 12 for more severe damage. Side effects at maintenance dose are typically absent.
Angiogenic signaling initiates: VEGF upregulation and actin sequestration begin facilitating immune and endothelial cell migration to injury sites. No measurable structural tissue changes at this timescale.
Little to no noticeable change in injury status. Some users report a general sense of reduced systemic inflammation. Fatigue and mild headache most commonly reported.
Angiogenesis and collagen deposition underway. New capillary formation at injury site supports oxygen and nutrient delivery. Anti-inflammatory signaling reduces pro-inflammatory cytokines.
Most users report noticeable improvement in pain, flexibility, and range of motion. Tendon and ligament injuries show the clearest early response at this stage. This is typically the first point where TB-500 is subjectively validated.
Accumulated angiogenic and tissue remodeling effects from loading. Fibrosis inhibition via myofibroblast differentiation suppression contributes to improved tissue quality and reduced scar formation.
Significant healing progress for most soft tissue injuries. Many users report substantially reduced pain and improved functional capacity. Some report near-full return to training.
Maintenance dosing preserves angiogenic stimulus at lower intensity. Tissue remodeling continues; collagen organization matures toward functional architecture.
Continued gradual improvement. Some cycle off at week 8 if injury is resolved; others continue to week 12 for complex injuries. Maintenance dose (2 mg 1×/week) is well-tolerated with minimal side effects.
Source: Estimated from animal PK data and limited human phase I data (PMID 34346165); no formal human PK characterization for TB-500 fragment
Loading the interactive decay curve.
TB-500 was classified as an FDA Category 2 bulk drug substance from 2024 until April 15, 2026, when HHS removed it along with 11 other peptides. Compounding pharmacy access is not yet available; PCAC review begins July 2026 with earliest access projected for late 2026 to mid-2027. All currently available supply in the US comes from gray-market research chemical vendors with no FDA quality oversight. The removal from Category 2 does not automatically legalize compounding. PCAC must review TB-500 before 503A/503B pharmacies can produce it. TB-500 has no FDA approval for any therapeutic indication. It has not completed any Phase II or Phase III clinical trial for the fragment form. WADA classifies TB-500 as S2 prohibited (Growth Factors), banned in and out of competition. A 4-year competition ban was issued in 2024 for documented use. US Department of Defense personnel are also prohibited from using TB-500. This content is for informational and research purposes only. It does not constitute medical advice, a prescription, or an endorsement of any product or protocol. Consult a licensed healthcare provider before using any research peptide.
Peptide Schedule Research TeamReviewed Apr 202610 Citations
