Combining BCMAxCD3 and anti-CD38 antibodies restores T cell activity in multiple myeloma and improves tumor cell killing.
Selective HDAC6 inhibitors improve isoform specificity to reduce off-target toxicity while increasing cancer cell sensitivity to radiotherapy and chemotherapy.
Selective arginase inhibitors restore tumor L-arginine levels to boost T-cell activation while limiting off-target effects and translation complexity.
Combining an anti-CD38 antibody, corticosteroid, and chemotherapy helps overcome drug resistance, improve remission, and reduce relapse risk.
A54 targets the HBD-II region of heparanase to block enzymatic activity and cell invasion while avoiding off-target effects of less specific inhibitors.
Selective LMP7 and LMP2 inhibition preserves therapeutic efficacy while reducing side effects linked to non-selective proteasome blockers.
Small-molecule TEAD inhibitors disrupt YAP-TAZ binding to curb tumor growth while limiting off-target effects and preserving normal cell functions.
Combining a CDK inhibitor with a BCL-2 or proteasome inhibitor improves anti-cancer response by boosting apoptosis and overcoming drug resistance.
Novel Formula I compounds selectively inhibit c-Myc, addressing drug resistance and limited treatment effectiveness in cancer and related diseases.
Reversible boronic acid binding selectively inhibits chymotrypsin-like proteasome activity, reducing side effects and resistance risk.
A four-drug BCMA-based regimen improves survival and minimal residual disease negativity in transplant-ineligible newly diagnosed myeloma.
Combining immuno-DASH inhibitors with PGE2 antagonists raises tolerated dose and antitumor immune response while reducing toxicity.
An injectable hyaluronic acid hydrogel forms a wet-surface barrier while reducing oxidative stress and inflammation to limit postoperative adhesions.