spec sheet11 rows
TP-508, known in development as Chrysalin and later given the name rusalatide acetate, is a synthetic 23-amino-acid peptide that copies the receptor-binding domain of human alpha-thrombin. It is a tissue-repair peptide, not a nootropic; the appeal is regenerative. Unlike whole thrombin it has no enzymatic activity, so it does not clot blood; instead it binds a distinct class of cell-surface thrombin receptors and kicks off a cascade of healing signals, including angiogenesis (new blood vessel growth), recruitment of inflammatory and progenitor cells, chemotaxis, and cell proliferation. It has been through real animal work and several human trials in diabetic foot ulcers and distal radius fractures, plus preclinical work in bone regeneration, cartilage repair, heart revascularization, and as an emergency radiation countermeasure. The clinical record is genuinely mixed; early studies looked promising, but the pivotal Phase III fracture trial missed its main clinical endpoint.
- Wound healing accelerated in a placebo controlled trial
- Strongly angiogenic; new blood vessels grow
- Fracture and bone repair speed up
- Blood flow improves through nitric oxide signaling
- Wakes up stem and progenitor cells
- Pure tissue repair; zero clotting activity
- TP-508 is literally a piece of your own thrombin; it copies the receptor-binding domain of human alpha-thrombin but leaves out the enzyme part, so it can trigger repair signals without clotting blood.
- It is a 23-amino-acid peptide, sequence AGYKPDEGKRGDACEGDSGGPFV (C-terminally amidated), and carries the formal drug name rusalatide acetate.
- Its headline effect in study after study is angiogenesis; wounds, fractures, and ischemic hearts treated with TP-508 consistently show more and larger new blood vessels.
- A single injection given 24 hours after a lethal radiation dose helped mice survive by protecting and reactivating intestinal crypt stem cells, which is why it was explored as a nuclear-incident countermeasure.
- Despite promising early trials, the big Phase III distal radius fracture study missed its primary clinical endpoint, which is the main reason you have never seen it on a pharmacy shelf.
Mechanism
TP-508 represents a portion of the receptor-binding domain of native human alpha-thrombin (a roughly 23-residue stretch around residues 508 to 530). During normal injury, thrombin is generated at the wound and its non-enzymatic tissue-repair functions are attributed to this domain. The reproduces those functions without the clotting activity. It binds to a specific class of high-affinity, non-proteolytically-activated thrombin receptors found on fibroblasts, endothelial cells, and other repair cells; this is a separate mechanism from the proteolytic tethered- activation of PAR1 that whole thrombin uses.
Downstream, TP-508 drives endothelial chemotaxis and new vessel growth, activates endothelial synthase (eNOS) and nitric oxide signaling to improve perfusion and reverse endothelial dysfunction, and promotes cell proliferation and survival through the PI3-kinase/ pathway.
In fracture models it up-regulates early growth factors, inflammatory mediators, and angiogenesis-related genes, and tips the balance of signaling toward cell growth over cell death (touching cell-cycle, JAK/STAT, NF-kB, PDGF, PTEN, and ERK/MAPK programs). In the gut it activates radioresistant crypt stem cells (DCLK1, LGR5) and preserves crypt integrity. The through-line is the same: it accelerates revascularization and regeneration rather than acting as a growth factor itself.
receptor fingerprint
Angiogenesis gene program (early growth factors, angiogenic and inflammatory mediators)Up-regulates
Non-proteolytically-activated thrombin receptor (fibroblast/endothelial high-affinity site)Agonist / binder
PI3-kinase / pathwayActivates (downstream)
Endothelial synthase (eNOS) / nitric oxide signalingUp-regulates
Dosingtypical ranges, not medical advice
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Safetyrisks and cautions, not medical advice
Across the published human trials TP-508 was reported as well tolerated. In the placebo-controlled diabetic foot ulcer study, local wound reactions and adverse events were equal between the peptide and placebo groups, with no reported drug-related changes in laboratory tests and no serious adverse events attributed to the drug. Because the peptide has no enzymatic thrombin activity, it does not itself promote clotting the way whole thrombin would. That said, the safety picture comes from relatively small, mostly local or topical dosing (micrograms applied to a wound bed or fracture site), not from long-term systemic use, so the real-world safety of self-administration is not established. This is an investigational peptide that was never approved for any indication; it is not a supplement and there is no vetted consumer dosing. Anyone considering it is operating well outside the evidence.
Reconstitutionarithmetic only, not dosing advice
arithmetic only; not medical or dosing advice.
History
TP-508 came out of work on the tissue-repair functions of thrombin and was developed by Chrysalis BioTechnology, which is where the trade name Chrysalin comes from. It was licensed to OrthoLogic Corp, which ran much of the orthopedic program. The peptide received the United States Adopted Name rusalatide acetate around 2005. Early human studies were encouraging: a Phase I/II diabetic foot ulcer trial showed dose-dependent improvements in healing, and a Phase I/II distal radius fracture study suggested accelerated fracture repair. The program then advanced to one of the larger Phase III fracture trials of its time in distal radius fractures.
That trial showed significant acceleration of radiographic healing but failed to meet its primary clinical endpoint (time to removal of immobilization) in the overall intent-to-treat population; a subset analysis suggested benefit in osteopenic women. That miss effectively ended the orthopedic commercialization push. The peptide continued in academic and government-adjacent research, notably by Chrysalis BioTherapeutics, as a regenerative agent and as a potential emergency countermeasure for radiation-induced gastrointestinal injury.
Reputation
In peptide and regenerative-medicine circles TP-508 is respected as a real, well-characterized molecule with a substantial peer-reviewed literature behind it, which sets it apart from a lot of the peptides sold online. It is talked about for wound healing, fracture and bone repair, and angiogenesis. The honest read is that it is a cautionary tale as much as a success story: the mechanism is well supported and the early trials looked good, but the pivotal fracture trial missed its main endpoint and the drug never reached approval. It is not a lifestyle or cognitive compound and has essentially no track record as a consumer product; interest today is niche and research-driven.
Subjective profileweighing the evidence above
Better evidenced than most repair peptides; a placebo-controlled diabetic foot ulcer trial is real human data, and it was well tolerated there. Everything else is animal work, it was never approved, and no vetted consumer dose exists, so treat it as an investigational tissue-repair agent rather than a recovery supplement.
Where to buy
Suppliers
Vendors carrying TP-508, with live product details and codes. Links are affiliate links that support the wiki at no cost to you.
RUO
TP-508
Research
- 2000first citedThrombin peptide, TP508, stimulates angiogenic responses in animal models of dermal wound heali…
- 2007controlled trialThrombin peptide Chrysalin stimulates healing of diabetic foot ulcers in a placebo-controlled p…
- 2015most recentNovel regenerative peptide TP508 mitigates radiation-induced gastrointestinal damage by activat…
- 1.Thrombin peptide Chrysalin stimulates healing of diabetic foot ulcers in a placebo-controlled phase I/II study.
- 2.Could rusalatide acetate be the future drug of choice for diabetic foot ulcers and fracture repair?
- 3.Thrombin peptide TP508 stimulates cellular events leading to angiogenesis, revascularization, and repair of dermal and musculoskeletal tissues.
- 4.Thrombin peptide, TP508, stimulates angiogenic responses in animal models of dermal wound healing, in chick chorioallantoic membranes, and in cultured human aortic and microvascular endothelial cells.
- 5.Repair of rabbit segmental defects with the thrombin peptide, TP508.
- 6.Thrombin peptide (TP508) promotes fracture repair by up-regulating inflammatory mediators, early growth factors, and increasing angiogenesis.
- 7.TP508 accelerates fracture repair by promoting cell growth over cell death.
- 8.Bone formation is enhanced by thrombin-related peptide TP508 during distraction osteogenesis.
- 9.TP508 (Chrysalin) reverses endothelial dysfunction and increases perfusion and myocardial function in hearts with chronic ischemia.
- 10.Thrombin peptide (TP508) promotes adipose tissue-derived stem cell proliferation via PI3 kinase/Akt pathway.
- 11.Novel regenerative peptide TP508 mitigates radiation-induced gastrointestinal damage by activating stem cells and preserving crypt integrity.
- 12.Evaluation of early osteochondral defect repair in a rabbit model utilizing fourier transform-infrared imaging spectroscopy, magnetic resonance imaging, and quantitative T2 mapping.
12 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Is TP-508 a nootropic?
No. It is a tissue-repair and angiogenesis peptide. Its documented effects are on wound healing, bone and fracture repair, blood vessel growth, and endothelial function, not on cognition or mood.
Does TP-508 cause blood clots since it comes from thrombin?
It represents only the non-enzymatic receptor-binding domain of thrombin, so it lacks the clotting enzyme activity of whole thrombin. It triggers repair signaling without the proteolytic clotting function, and trials did not report it as a clotting risk.
Was TP-508 ever approved as a drug?
No. It advanced through Phase I/II trials in diabetic foot ulcers and distal radius fractures with encouraging results, but the pivotal Phase III fracture trial missed its primary clinical endpoint and the drug was never approved for any indication.
What is the strongest evidence for TP-508?
The most consistent finding across dermal, bone, and cardiac models is angiogenesis and revascularization. On the clinical side, the placebo-controlled diabetic foot ulcer study is the standout positive human trial; the fracture program is where the evidence turned mixed.
Why was TP-508 studied for radiation exposure?
In mice, a single injection 24 hours after a lethal radiation dose improved survival by protecting intestinal crypts and reactivating radioresistant stem cells (DCLK1, LGR5). That made it a candidate emergency countermeasure for the gastrointestinal syndrome after nuclear exposure.
Limitations of the evidence
- Investigational peptide, never approved; no vetted consumer dosing and no long-term human safety data
Notes and cautions
- Human evidence is mixed; the pivotal Phase III distal radius fracture trial missed its primary clinical endpoint
- Most safety data comes from small, local or topical dosing, not systemic self-administration
- Sourced peptide from gray-market vendors carries the usual purity, sterility, and dosing-accuracy risks