Captor Therapeutics ®

Pipeline

Target
Indications
Modality
Discovery
Preclinical*
IND Filing
Phase IA / IB
  • GSPT1, NEK7, SALL4
    Hepatocellular carcinoma, Lung cancer, NET tumours
    MG

    Project description GSPT1, NEK7, SALL4

    GSPT1 (G1 to S phase transition 1 protein) is a translation termination factor critical for the release of nascent polypeptides from ribosomes. Translational adaptations are crucial components of cancer development and progression, as rapid and continuous proliferation of highly malignant cancers requires efficient protein synthesis. Number of different cancers, including liver, lung or breast cancers are highly sensitive to GSPT1 degradation. NEK7 (NIMA-related kinase 7)  is a serine/threonine kinase, whose dysregulation leads to abnormal production of IL-1b. In the context of cancer, high level of IL-1b in tumor microenvironment play strong immunosuppressive role. SALL4 is a transcription factor present in the cancer stem cells (CSCs), that regulates their functions. It therefore plays a significant role in the carcinogenesis and progression of HCC.  Degradation of SALL4 would allow to eliminate the CSC and achieve a long lasting therapeutic effect.

    The molecule developed by Captor:

    1. Is a triple degrader of GSPT-1, NEK7 and SALL4 proteins
    2. Demonstrates high efficacy across Cell Line-Derived and Patient-Derived HCC Xenograft models
    3. Shows strong synergy in combination with everolimus
    4. Is a prodrug with enhanced tissue specificity towards liver and lung cancers
     

    Files to download

    Not applicable

  • NEK7
    Brain-penetrant: Neuroinflammation (Parkinson's Disease, ALS, MS)
    MG

    Project description NEK7

    NEK7 belongs to the protein kinase family and serves as the key regulator of NLRP3 inflammasome activation pathway. There is growing evidence of the role of pathological activation of the innate immunity in the pathogenesis of neurodegenerative diseases (NDDs), however, limited treatment strategies are currently available. NEK7's pathological significance results primarily from its structural role rather than its enzymatic function, presenting considerable challenges in the development of traditional kinase inhibitor drugs.


    Drugs developed by Captor:

    1. Eliminate all pathological functions of NEK7 related to the regulation of the NLRP3 pathway through its complete degradation.
    2. Demonstrate almost 100% degradation of the NEK7 protein in Macaca fascicularis monkeys for over 20 hours after oral administration.
    3. They are capable of crossing the blood-brain barrier.
    4. May be applicable in the therapy of NDDs characterized by neuroinflammation, such as Parkinson's disease, Alzheimer's disease, Amyotrophic Lateral Sclerosis, or Huntington's disease. 

  • NEK7
    Systemic: Autoimmunity (IBD, Gout, Dermatological diseases)
    MG

    Project description NEK7

    NEK7 is a protein from the family of protein kinases and the main regulator of NLRP3 inflammasome activation. Disturbances in the activity of the NLRP3 pathway can lead to the development / progression of autoimmune diseases and chronic inflammatory conditions. The pathological role of NEK7 arises from its structural rather than enzymatic function, significantly complicating the development of classical kinase inhibitor drugs. 

    Drugs developed by Captor:

    1. Eliminate all pathological functions of NEK7 related to the regulation of the NLRP3 pathway through its complete degradation.
    2. They are characterized by excellent pharmacokinetics properties (PK) providing prolonged exposure to the compound.
    3. Demonstrate almost 100% degradation of the NEK7 protein in Macaca fascicularis monkeys for over 20 hours after oral administration.
    4. May find application in the therapy of autoimmune diseases, disorders related to metabolic diseases and obesity, as well as cardiovascular diseases.

  • PKCӨ
    Autoimmunity, Oncology, Transplantation, Metabolism
    BID

    Project description PKCӨ

    Protein Kinase C theta (PKC-θ) is a serine/threonine kinase selectively expressed in T cell, NK cell and skeletal muscles. Blocking the proliferation and activation of T lymphocytes is an attractive therapeutic approach in the treatment of autoimmune diseases (e.g. IBD, psoriasis, RA). Degradation of active PKC-θ extinguishes relevant signaling pathways resulting in downregulation of inflammatory cytokines production. Moreover, the most recent literature suggests that PKC-θ may be an important target in solid cancers (TNBC, GIST). Previous approach based on classical inhibitors was characterized by good efficacy in patients but numerous side effects resulting from inhibition of other PKC protein isoforms as well as other unidentified molecular targets due to selectivity issues. The use of TPD technology, and in particular the use of bifunctional degraders, allowed the development of molecules with the highest selectivity in this class.

    Captor’s bifunctional degraders:

    1. Degrade only the active PKC-θ form, present in activated, disease-driving cells.
    2. Are highly selective towards PKC-θ as well as in terms of the human kinome (KinomeScan test).
    3. Efficiently degrade 100% of PKC-θ protein in a mouse model of inflammation.

    Files to download

    Not applicable

  • New target projects
    Autoimmunity, Cancer
    MG BID

*Preclinical stage include IND-enabling studies, 

BID – Bi-functional Degrader; MG – Molecular Glue

Assumed stage at the end of 2025