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Antagonizing TSP1/CD36 Polypeptide Blocking the activation of TGF-β1

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  • Project profile
    Project name: Antagonizing TSP1/CD36 Polypeptide Blocking the activation of TGF-β1
    Indications: Progressive Fibrosis Interstitial Lung Disease (PF-ILD), Solid Tumor.
    Research phase: IND Approval in China
    Cooperation demands: Out-licensing outside the Great China
  • Highlights
    HTPEP-001: the first product from our polypeptide platform.
    1. Clear MoA. As an antagonist upstream of the TGF-β signaling pathway, HTPEP-001 mediates TGF-β1 activation by completely inhibiting the binding of TSP-1 and CD36, reducing multiple profibrotic factors expression.

    2. Treat fibrosis sequelae of COVID-19. A systematic review and meta-analysis shows approximately 20% of COVID-19 patients, at least 48 million people, have evidence of fibrotic sequelae persisting at 1-year follow-up. As a pan-anti-fibrotic drug, HTPEP-001 is a good therapeutic option for the sequelae.

    3. Effectiveness. Compared with Nintedanib by head-to-head assay in vivo, HTPEP-001 displays better therapeutical efficacy for lung fibrosis.


    OFev: Nintedanib


    4. Safety. HTPEP-001 shows significant safety advantages over existing and developing treatment options.


    5. Wide range of indications. At first, HTPEP-001 is an effective therapeutic method for fibrosis diseases, especially lung fibrosis. Besides, the studies in vivo show HTPEP-001 combined with anti-PD-1 mAb enhances the anti-tumor efficacy.

    (43% higher than anti-PD-1)


    6. Great market prospect. There is huge unmet clinical needs in the field of fibrotic diseases, and HTPEP-001 meets the needs with a great market prospect.

    7. Dosage form variety. HTPEP-001 is available for both intravenous and inhalation routes of administration, to meet the needs of different stage of PF-ILD patients.
  • Project Introduction

    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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