(43% higher than anti-PD-1)
1. Asset type：Antagonizing TSP1/CD36 Polypeptide.
2. Dosage form: Injection or Nebulization.
3. Mechanism of action：TGF-β1 is a central player in fibrosis and cancer diseases. TSP1, a multi-functional matricellular ECM, is upregulated expression in tissue injury and repair. TSP1 binds to CD36, and then binding to latent TGF-β complex converts latent TGF-β to its biologically active form through a non-proteolytic mechanism. TSP1 binding to CD36 was required for TGF-β activation. HTPEP-001 peptide competitively binds to TSP1 to block the binding of TSP1 and CD36，leading to inhibit TGF-β1 activation.
4. Indication：Progressive Fibrosis Interstitial Lung Disease (PF-ILD), Solid Tumor. Note：PF-ILD: Including idiopathic pulmonary fibrosis (IPF), connective tissue disease-related interstitial lung disease (CTD-ILD), pneumoconiosis, Sarcoidosis, viral infectious interstitial lung disease with progression of pulmonary fibrosis.
5. Research phase: IND Approval in China.
6. Research progress：
1) The pre-clinical pharmacodynamics study has been completed. Compared with nintedanib in rats induced fibrosis by bleomycin, HTPEP-001 displays obvious better therapeutic effect for IPF than Nintedanib.
2) The pre-clinical study in rats, beagles and cynomolgus monkey have been completed. They show no obvious adverse effects, and HTPEP-001 possessing the margin of safety about 100 folds that is significantly better than nintedanib.
3) Manufacturing of the HTPEP-001 is a stable and highly qualified process, formulations of both inhalation and infusion solutions are well characterized and controlled.
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