the potential of the PKCӨ protein pathway is underpinned by BMS's latest in-licensing of Exscientia's PKCӨ inhibitor EXC4318.The IL-17 pathway is a clinically validated pathway in autoimmune diseases such as psoriasis with established modulators 2 the PKCӨ protein acts via the CD3/CD28 – IL-2/IL-17 pathway.Importantly, the approach behind CT-05 is partially de-risked thanks to: PKCӨ is a high-value target with opportunities in certain autoimmune diseases, such as allergy, psoriasis, and inflammatory bowel disease, as well as certain malignancies, such as breast and gastrointestinal cancer. It is therefore expected that degrading the PKCӨ protein would lead to an increased T cell suppressive function. Indeed, PKCӨ plays an important role in the modulation of T cells by limiting the suppressive function of T cells. Compounds with the ability to cross the blood-brain-barrier have been identified and provide opportunity for further development in the area of neurodegenerationĬT-05 targeting (new disclosure) PKCӨ (PKC theta)ĬT-05 targets the PKCӨ protein, a protein highly relevant in both autoimmune diseases and cancer.Optimised compounds with good pharmacokinetics in animals have been developed.Degradation of NEK7 is correlated with the desired in-vitro biological effects on the inflammatory response.Effective NEK7 degradation at low concentrations in vitro (high potency) and ex vivo.Pre-clinical studies have revealed the following benefits of CT-02: It is therefore expected that selective degradation of NEK7 would also remove the NEK7 scaffolding function leading to potent inflammatory inhibition. Importantly, it is established that NEK7 pro-inflammatory activity is largely driven by its scaffolding function, and because of that, classical inhibition of NEK7's kinase function doesn't provide therapeutic benefit. Such NEK7 degradation allows the modulation of the inflammasome, a complex that plays a critical role in the regulation of the inflammatory response.Ĭaptor believes that selective NEK7 degraders have the potential to overcome the limitations shown in the past of NLRP3 inhibitor drugs related to increased susceptibility to infection. In addition to the potential benefits of NEK7 degradation combined with the degradation of GSPT1 and SALL4 in cancer, as mentioned above for the CT- 01 Project, the selective degradation of NEK7 alone in the CT-02 Project has many potential benefits as a treatment of several autoimmune diseases. Moreover, CPT-6281 is particularly well suited for liver, lung, and neuroendocrine tumors since it is a prodrug 1 activated by an enzyme present in high concentration in the liver, the lungs, and some gastrointestinal tumors. GSPT1 is a protein involved in the termination of translation, SALL4 is a transcription factor often over-expressed in HCC patients and correlating with poor prognosis, and NEK7 is a protein in which degradation leads to a reduction in IL-1b production, a well-known pro-carcinogenic factor. The first indication will be in Hepatocellular Carcinoma (HCC).ĬPT-6281 is a first-in-class degrader of GSPT1, SALL4, and NEK7.
#CAPTOR THERAPEUTICS TRIAL#
Webcast invitation to discuss scientific rational and market potential of new targetsĭate: March 30 th 2023 at 4pm CET / 10 am ETĬT-01 / CPT-6281 targeting GSPT1, SALL4 and (new disclosure) NEK7ĬT-01 / CPT-6281 is currently undergoing IND/CTA-enabling studies with the first clinical trial expected to start at the end of 2023.
#CAPTOR THERAPEUTICS UPDATE#
("Captor") CTX, a leader in the development of Targeted Protein Degradation (TPD)-based drugs, today discloses the identity of the drug targets as well as associated supporting data, and provides an update on the progress in the research and development of its pipeline lead programs CT-01, CT-02 and CT-05.ĭr Michal Walczak, Chief Scientific Officer and Co-founder of Captor, will present the scientific rational for these targets as well as the market potential of each of Captor's lead programs and will answer questions during a webcast on March 30 th 2023. WROCŁAW, Poland, Ma(GLOBE NEWSWIRE) - Captor Therapeutics S.A.
#CAPTOR THERAPEUTICS REGISTRATION#
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