P1/2, N=16, Recruiting, Misty Shields | Not yet recruiting --> Recruiting | Initiation date: May 2026 --> Aug 2026

P3, N=422, Recruiting, Nantes University Hospital | Not yet recruiting --> Recruiting | Trial completion date: Jan 2031 --> Jun 2031 | Initiation date: Jan 2026 --> Jun 2026 | Trial primary completion date: Jul 2030 --> Dec 2030

P2, N=9, Active, not recruiting, Cancer Institute and Hospital, Chinese Academy of Medical Sciences | Not yet recruiting --> Active, not recruiting | Trial completion date: Dec 2025 --> Jun 2027 | Trial primary completion date: Mar 2025 --> Dec 2026

P2, N=69, Not yet recruiting, Yonsei University

P2/3, N=345, Active, not recruiting, Pharma Mar S.A. | Recruiting --> Active, not recruiting

While modulating Bcl-2 pathways can be effective in MS, future research should aim to provide greater clarification and to design precision-based drugs capable of neuroprotective effects.

Among 5 255 randomized patients, 374 (7.1%) had LTBI and received preventive treatment, most commonly isoniazid (82.1%) and rifampicin (11.8%). From Year 1-5 (after ~98% of LTBI+ patients completed preventive treatment), transaminase elevations were generally similar among LTBI+ and LTBI- patients. The absence of observed TB risk in guselkumab-treated patients suggests IL-23 inhibitors may be better treatment options than TNFi in high-risk patients, including those in TB-endemic regions.

From approval of immune checkpoint inhibitors and lurbinectedin, a newer chemotherapy agent, to novel immunotherapies such as tarlatamab, a DLL3-CD3 bispecific T-cell engager, and other upcoming promising drugs, the therapeutic armamentarium for SCLC is steadily expanding. In this study, we review the current landscape of both systemic therapy as well as radiation therapy for SCLC, with a focus on major developments over the past decade, current standards of care, and novel therapeutics that are expected to revolutionize the treatment of this aggressive malignancy.

Only inhibition of CDK9 (by AZD4573 and atuveciclib) or of CDK12/13 (by SR4835 and THZ531)-which target the transcriptional elongation of RNA polymerase II (RNAPII)-exerted a strong apoptotic potential. Because Bcl-2 only inhibits Bax, but not Bak, AZD4573 and SR4835 were able to induce apoptosis in Jurkat cells overexpressing Bcl-2. As tumor cells frequently upregulate Bcl-2, inhibitors of CDK9 and CDK12/13 represent promising anticancer drugs.

Silibinin and sodium oxamate, as HIF-1α and LDHA blockers, respectively, were used to treat K-562 and HL-60 cells...In contrast, PD-L1 expression remained unchanged after treatment. Our findings suggest that blocking signaling pathways involved in metabolic reprogramming of cancer cells could be a promising approach for modulating the expression of certain immune checkpoint ligands, warranting further investigation.

P3, N=455, Active, not recruiting, PharmaMar | Recruiting --> Active, not recruiting

P3, N=705, Completed, PharmaMar | Active, not recruiting --> Completed