eligibility_summary
Inclusion: 15-74, relapsed/refractory or non-CR MM after 4 cycles, KPS>=50/ECOG<=2, ANC>1.0, Plt>50, Lym>=0.15, ALT/AST<3xULN, Tbili<1.5, Cr<2.5 or CrCl>=60, EF>=45%, SpO2>=92%, not pregnant, contraception. Exclusion: short survival/rapid PD, other active cancers, uncontrolled infection or HIV/HBV/HCV, CNS disease, recent serious cardiac disease, anticoagulation/coagulopathy, interacting drugs/allergy, recent systemic steroids, poor T-cell transduction, other trials, pregnancy/lactation.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: CD38/CS1 dual‑target CAR‑T cell therapy (autologous, biological IV infusion). Mechanism: patient T cells are genetically engineered to express a chimeric antigen receptor that co‑recognizes CD38 and CS1 (SLAMF7) on myeloma cells, CAR signaling triggers T‑cell cytotoxicity (perforin/granzyme, cytokines). Dual targeting broadens tumor recognition and reduces antigen‑loss escape, maintaining activity against CD38+, CS1+, or double‑positive clones (>80% kill in preclinical assays). Targets: malignant plasma cells in relapsed/refractory multiple myeloma expressing CD38 and/or CS1, relevant pathways include CD38 ectoenzyme/NADase and SLAMF7 signaling, immune effector pathway via CAR (CD3ζ with costimulation). Early Phase 1, single‑arm, status active, not recruiting (China).