Senhwa Biosciences Inc (TPEx: 6492), a Taiwan-based drug development company involved in therapeutics for oncology, rare diseases, and infectious diseases, announced on Tuesday that its new drug Pidnarulex (CX-5461) has been selected by the US National Cancer Institute (NCI) as part of a five-year cancer research programme.

The first patient in the monotherapy clinical trial for advanced solid tumours has been successfully enrolled at the NIH Clinical Center in Bethesda, Maryland. The NCI will fund the full cost of the clinical trial, estimated at approximately USD4.8m.

In addition to this initial monotherapy trial, three other clinical studies led and sponsored by NCI are in progress. These include combination therapies with immunotherapy, antibody-drug conjugates (ADCs), and a monotherapy study targeting MYC-driven lymphomas. IND submissions and patient enrolment for these additional studies are expected to begin shortly.

The first trial in the NCI programme will investigate CX-5461 as a single agent in patients with and without homologous recombination deficiency (HRD) gene mutations, evaluating its ability to induce the Rad51 response. The study also aims to identify additional biomarkers associated with synthetic lethality to help define patient populations more likely to respond to treatment and potentially expand its clinical indications. The trial is planned to enrol 40 patients, with allocated resources including clinical site operations, pharmacokinetic (PK) and biomarker analyses, as well as execution costs such as regulatory compliance, data management, and electronic platform infrastructure. With full financial support from NCI, the trial is expected to save the company an estimated USD4.8m in clinical development costs, significantly reducing the R&D burden and accelerating the advancement of CX-5461.

CX-5461 is a first-in-class small molecule drug with a unique mechanism of action. It acts by selectively targeting and stabilising G-quadruplexes (G4s), preventing their unwinding and triggering replication-dependent DNA damage, ultimately resulting in cancer cell apoptosis.