PARP Inhibitor Development

PARP Inhibitor Development

Poly(ADP-ribose) polymerase (PARP) inhibitors have emerged as a transformative therapeutic approach in the management of breast cancer, particularly for patients harboring deleterious mutations in the BRCA1 and BRCA2 genes. At Alfa Cytology, we specialize in the preclinical discovery of PARP inhibitors and promotes the development of new therapies for breast cancer.

Introduction to PARP Inhibitor for Breast Cancer

The underlying principle behind PARP inhibitor therapy lies in the concept of "synthetic lethality." PARP enzymes are responsible for the base excision repair (BER) pathway, which mends single-strand breaks in DNA. In the absence of functional BRCA1 or BRCA2 proteins, cancer cells become highly dependent on the PARP-mediated BER pathway for survival. By inhibiting PARP activity, these DNA single-strand breaks accumulate and ultimately lead to the formation of lethal double-strand breaks, triggering apoptosis selectively in the BRCA-deficient tumor cells.

Fig. 1 PARP inhibitors suppress PARP catalytic activity and cause cell death in tumors. (Demir Cetinkaya B., et al. 2022)Fig. 1 PARP inhibitors (olaparib and talazoparib) suppress PARP catalytic activity and cause cell death in tumors with BRCA1 and BRCA2 mutations. (Demir Cetinkaya B., et al. 2022)

PARP Inhibitor Development for Breast Cancer

The remarkable efficacy and favorable safety profile of PARP inhibitors have made them a transformative addition to the breast cancer treatment landscape, particularly for patients with BRCA-mutated disease. Ongoing research aims to build upon these successes and further optimize the use of these targeted therapies.

NCT Targets Therapeutics Phase
NCT05582499 PARP inhibitor + CDK
inhibitor
Fluzoparib + dalpiciclib/fluzoparib + chemotherapy
NCT05332561 PARP inhibitor Olaparib
NCT05761470 PARP inhibitor + IO Fluzoparib + camrelizumab + chemotherapy
NCT02849496 PARP inhibitor + IO Olaparib + atezolizumab
NCT04481113 PARP inhibitor + CDK
inhibitor
Niraparib + abemaciclib
NCT05834582 PARP inhibitor Fluzoparib + chemotherapy
NCT03911453 PARP inhibitor Rucaparib
NCT05498155 PARP inhibitor + IO Olaparib ± durvalumab
NCT045842555 PARP inhibitor + IO Olaparib ± durvalumab

Our Services

As a leading preclinical CRO, Alfa Cytology is committed to advancing the development of innovative cancer therapies, including PARP inhibitors for breast cancer. Our state-of-the-art facilities and multidisciplinary team of experts provide comprehensive services to support the entire drug development process, from target identification and validation to preclinical studies and biomarker development.

Selective Inhibitor
Development

  • PARP-1 Selective Inhibitor Development
  • PARP-2 Selective Inhibitor Development
  • PARP-3 Selective Inhibitor Development
  • PARP-5 Selective Inhibitor Development
  • PARP-7 Selective Inhibitor Development
  • More

PARP Degrader (PROTAC) Development

PARP Inhibitor Development for Breast Cancer

PARP Peptide Inhibitor Development

Dual inhibitor
Development

  • PARP/HDAC Dual Targeting Inhibitor Development
  • PARP/PI3K Dual Targeting Inhibitor Development
  • PARP/EGFR Dual Targeting Inhibitor Development
  • PARP/EZH2 Dual Targeting Inhibitor Development
  • PARP/PI3K Dual Targeting Inhibitor Development
  • More

Alfa Cytology provides development services for PARP inhibitors, covering drug design, screening, and efficacy research to find ideal drug candidates for you and accelerate preclinical research on your breast cancer therapeutics. To learn more about our capabilities in PARP inhibitor development for breast cancer or to discuss potential collaborative opportunities, please don't hesitate to contact us.

Reference

  1. Demir Cetinkaya B., Biray Avci C. Molecular perspective on targeted therapy in breast cancer: a review of current status. Med Oncol. 2022, 39(10): 149.
All our services and products are exclusively intended for preclinical research purposes. They are not intended for diagnostic, therapeutic, or patient management applications.