The British Columbia Cancer Agency recently discussed their research efforts toward the discovery of new radiotherapeutic agents for the treatment of prostate cancer.
At the recent EANM meeting, Point Biopharma Global Inc. presented preclinical details on the development of 177Lu-PNT2001 and 225Ac-PNT2001 for the treatment of prostate cancer.
The suboptimal metabolic stability of radiolabeled gastrin-releasing peptide receptor (GRPR) antagonists has been a hindering factor of these promising theranostic candidates for prostate cancer. Uppsala University researchers have recently reported the development of [111In]DOTAGA-PEG-2-SAR11-RM-26, after replacement of Gly11 by Sar11 in the peptidic chain.
At the recent European Association of Nuclear Medicine meeting in Barcelona, researchers from the British Columbia Cancer Research Institute and the University of British Columbia reported the development and preclinical evaluation of bispecific radiotracers designed to target prostate-specific membrane antigen (PSMA) and fibroblast activation protein (FAP).
Medshine Discovery Inc. has presented furan fused ring-substituted glutarimides as proteolysis targeting chimera (PROTAC) compounds comprising an E3 ubiquitin ligase-binding moiety covalently linked to androgen receptor-targeting moiety reported to be useful for the treatment of prostate cancer.
University of Michigan has described new proteolysis targeting chimeric (PROTACs) compounds comprising cereblon (CRBN) ligands covalently bonded to CREB-binding protein (CBP) and/or histone acetyltransferase KAT3B (p300)-targeting moiety through linker reported to be useful for the treatment of cancer.
A Mayo Clinic study demonstrated how the deficiency of the enzyme CDK12 or its regulation by cyclin K causes the expression of mutations related to resistance to endocrine therapy in prostate cancer. Prostate tumors with CDK12 deficiency are more aggressive, recurrent, produce metastases and are associated with castration-resistant prostate cancer (CRPC). CDK12 deficiency impairs DNA repair and increases genomic instability, causing an effect known as homologous recombination deficiency or BRCAness.
