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Captor Therapeutics Discloses Molecular Targets of Pipeline’s Lead Assets and Invites Stakeholders to Webcast

27.03.2023
  • CT-01 targets 3 well suited proteins including NEK7 with poor prognosis in key liver cancer
  • Strong preclinical data generated with CT-02 against NEK7
  • CT-05 potential best-in-class profile in high potential / partially     de-risked PKCӨ protein pathway
  • Webcast to take place on Thursday 30th March at 4 pm CET / 10 am ET – Registration link below

 

Wrocław, Poland, March 27, 2023. - Captor Therapeutics S.A. (“Captor”) (WSE: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.

Dr 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 30th 2023.

Webcast invitation to discuss scientific rational and market potential of new targets

Date: March 30th 2023 at 4pm CET / 10 am ET

Please register by following this link.

CT-01 / CPT-6281 targeting GSPT1, SALL4 and (new disclosure) NEK7

CT-01 / CPT-6281 is currently undergoing IND/CTA-enabling studies with the first clinical trial expected to start at the end of 2023. The first indication will be in Hepatocellular Carcinoma (HCC).

CPT-6281 is a first-in-class degrader of GSPT1, SALL4, and NEK7. 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.

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.

CT-02 targeting (new disclosure) NEK7

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. Such NEK7 degradation allows the modulation of the inflammasome, a complex that plays a critical role in the regulation of the inflammatory response.

Captor 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. 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. It is therefore expected that selective degradation of NEK7 would also remove the NEK7 scaffolding function leading to potent inflammatory inhibition.

Pre-clinical studies have revealed the following benefits of CT-02:

  • Effective NEK7 degradation at low concentrations in vitro (high potency) and ex vivo
  • Degradation of NEK7 is correlated with the desired in-vitro biological effects on the inflammatory response
  • Optimised compounds with good pharmacokinetics in animals have been developed
  • Compounds with the ability to cross the blood-brain-barrier have been identified and provide opportunity for further development in the area of neurodegeneration

CT-05 targeting (new disclosure) PKCӨ (PKC theta)

CT-05 targets the PKCӨ protein, a protein highly relevant in both autoimmune diseases and cancer. Indeed, PKCӨ plays an important role in the modulation of T cells by limiting the suppressive function of T cells. It is therefore expected that degrading the PKCӨ protein would lead to an increased T cell suppressive function. 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.

Importantly, the approach behind CT-05 is partially de-risked thanks to:

  • the PKCӨ protein acts via the CD3/CD28 – IL-2/IL-17 pathway. The IL-17 pathway is a clinically validated pathway in autoimmune diseases such as psoriasis with established modulators[2]
  • the potential of the PKCӨ protein pathway is underpinned by BMS’s latest in-licensing of Exscientia’s PKCӨ inhibitor EXC4318

In preclinical studies, CT-05 has demonstrated attractive features that differentiate CT-05 from inhibitors that failed in clinical trials due to side effects:

  • Potent degradation and first-in-class selectivity profile of the molecular target PKCӨ in immune cells in vitro
  • Desired effect on ex vivo immune cells
  • No effect on non-immune cells

About Captor Therapeutics

Captor Therapeutics is a drug discovery and development company applying targeted protein degradation (TPD) technology to discover and develop breakthrough drugs for diseases with significant unmet medical need. TPD is a revolutionary approach to developing new drugs that can target new molecular targets considered undruggable" using classical drug modalities and provide additional treatment options for diseases where existing drugs do not provide optimal treatment. Captor is currently developing treatments for undertreated serious conditions, including cancer and autoimmune diseases.

 

For more information on Captor Therapeutics, visit: http://www.captortherapeutics.com

LinkedIn: @CaptorTherapeutics

Twitter: @CaptorTherapeu1

 

Media and investor contacts:

Polish Media and Investor Relations:

Point of View Bartosz Sawulski

+48 694 400 787

captorthercg05liapeutics@pov.pl

International Investor Relations:

LifeSci Advisors

Guillaume van Renterghem

+41 (0)76 735 01 31

gvanrenn925terghem@lifesciadvisors.co

 

 

[1] A prodrug is a biologically inactive compound which can be metabolized in the body to produce a drug which is pharmacological active.

[2] Ixekizumab, Secukinumab, Brodalumab

 

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