구조모아 (StructureMoa)항암 chemical structure spider web
방문프로그램 상세에서 관심 등록 후 2개 이상 모으면 여기서 한 번에 비교할 수 있습니다.
표가 넓으면 좌우로 스크롤하세요. 핵심 비교 모드에서는 중요 항목만 표시됩니다.
| 항목 | ciltacabtagene autoleucel (Carvykti, cilta-cel, LCAR-B38M, JNJ-68284528) Johnson & Johnson / Legend Biotech·BCMA 29 trials·t½ Cellular expansion kinetics rather than classical half-life | teclistamab (Tecvayli, JNJ-64007957, teclistamab-cqyv) Johnson & Johnson·BCMA × CD3 132 trials·t½ ~2–3 weeks at steady state | linvoseltamab (Lynozyfic, REGN5458, linvoseltamab-gcpt) Regeneron·BCMA × CD3 24 trials·t½ IgG-like, supporting weekly then less frequent dosing |
|---|---|---|---|
Overview Program | Carvykti (ciltacabtagene autoleucel) | Tecvayli (teclistamab) | Lynozyfic (linvoseltamab) |
Overview Company | Johnson & Johnson / Legend Biotech | Johnson & Johnson | Regeneron |
Overview Modality | CGT | ANTIBODY | ANTIBODY |
Overview Target | BCMA | BCMA × CD3 | BCMA × CD3 |
Overview Indication | Relapsed or refractory multiple myeloma | Relapsed or refractory multiple myeloma | Relapsed or refractory multiple myeloma after ≥4 prior lines including a PI, an IMiD, and an anti-CD38 antibody |
Overview Phase | APPROVED | APPROVED | APPROVED |
Overview Status | APPROVED | APPROVED | APPROVED |
Overview Content status | Curated Core | Curated Core | Curated Core |
Overview Data Confidence | Data Confidence · High | Data Confidence · High | Data Confidence · High |
Overview Development Signal | Development Signal · Established | Development Signal · Established | Development Signal · Established |
Overview Approval status | FDA approved | FDA approved | FDA approved |
Positioning Key differentiator | Dual-epitope BCMA binding raises avidity and appears to sustain CAR-T persistence longer than single-domain designs. | No manufacturing slot needed, so it can be started immediately in rapidly progressing myeloma. | Response-adapted schedule can stretch to q4w after a deep response, so the compare with Tecvayli is visit burden and CRS step-up, not the antigen. |
Positioning Known limitation | BCMA loss or biallelic deletion, soluble BCMA shedding, T-cell exhaustion, and immunosuppressive marrow niche. | BCMA loss, soluble BCMA acting as a sink, and T-cell exhaustion. | BCMA loss or mutation, T-cell exhaustion, and prior BCMA-directed therapy. |
Positioning Development positioning | Best-in-class efficacy in BCMA CAR-T, ahead of Abecma on depth of response. | Class-defining BCMA engager; competes with Elrexfio and BCMA CAR-T. | Second approved BCMA engager after Tecvayli; dosing frequency is the operational split. |
Technology Vector | Lentiviral | — | — |
MoA Mechanism | Autologous T cells engineered with a dual-epitope BCMA CAR recognize BCMA on malignant plasma cells and trigger MHC-independent cytolysis and clonal CAR-T expansion. | Simultaneously engages BCMA on plasma cells and CD3 on T cells, forming an immune synapse that redirects polyclonal T cells to lyse BCMA+ myeloma cells independent of TCR specificity. | Binds BCMA on myeloma cells and CD3 on T cells, forming a cytolytic synapse that kills the plasma cell independent of native TCR specificity. |
MoA Biomarker | BCMA expression, MRD negativity at 10⁻⁵, CAR transgene persistence. | BCMA expression, MRD negativity, serum free light chain response. | BCMA expression is not a companion diagnostic; soluble BCMA is exploratory. |
PK/PD Half-life | Cellular expansion kinetics rather than classical half-life | ~2–3 weeks at steady state | IgG-like, supporting weekly then less frequent dosing |
PK/PD Species | Peak CAR transgene level, MRD negativity, soluble BCMA decline | Cynomolgus monkey, T-cell activation markers, cytokine profile, soluble BCMA | ORR, MRD, soluble BCMA |
PK/PD Animal (cat.) | Human | Human, NHP | Human |
PK/PD Experiment | PK | pharmacokinetic | — |
Toxicology Species | — | Mouse | — |
Toxicology Major finding | Boxed warnings for CRS, ICANS, parkinsonism and Guillain-Barré syndrome, HLH/MAS, prolonged cytopenia, and secondary T-cell malignancy. | Boxed warning for CRS and neurologic toxicity including ICANS. Profound hypogammaglobulinemia and infection — including opportunistic infection — drive most late morbidity. | Boxed warning for CRS and neurologic toxicity including ICANS. Neutropenia, infection, and hypogammaglobulinemia dominate later cycles. |
Toxicology CRS | CRS in ~95% of CARTITUDE-1 patients, grade ≥3 ~4% | CRS ~72%, grade ≥3 ~0.6% | CRS common, mostly grade 1–2 with step-up |
Clinical Safety signal | Boxed warnings for CRS, ICANS, parkinsonism and Guillain-Barré syndrome, HLH/MAS, prolonged cytopenia, and secondary T-cell malignancy. | Boxed warning for CRS and neurologic toxicity including ICANS. Profound hypogammaglobulinemia and infection — including opportunistic infection — drive most late morbidity. | Boxed warning for CRS and neurologic toxicity including ICANS. Neutropenia, infection, and hypogammaglobulinemia dominate later cycles. |
Clinical Selected reported efficacy | ORR 97% | ORR 63% | ORR 70% |
Clinical Reported ORR | 97% | 63.0% | 70% |
Clinical Reported PFS | HR 0.26 vs standard care in CARTITUDE-4 | ~11.3 mo | — |
Clinical Reported OS | NA | — | — |
Clinical Result source | CARTITUDE-1 (NCT03548207) / CARTITUDE-4 (NCT04181827) | MajesTEC-1 (NCT03145181 / NCT04557098) | LINKER-MM1 (NCT03761108) |
Clinical Program phase | APPROVED | APPROVED | APPROVED |
Clinical Trial activity | No active/completed counts | No active/completed counts | — |
Clinical Trial ref | NCT03548207 | NCT03145181 | NCT03761108 |
프로그램 상세에서 관심 등록 후 2개 이상 모으면 여기서 한 번에 비교할 수 있습니다.
표가 넓으면 좌우로 스크롤하세요. 핵심 비교 모드에서는 중요 항목만 표시됩니다.
| 항목 | ciltacabtagene autoleucel (Carvykti, cilta-cel, LCAR-B38M, JNJ-68284528) Johnson & Johnson / Legend Biotech·BCMA 29 trials·t½ Cellular expansion kinetics rather than classical half-life | teclistamab (Tecvayli, JNJ-64007957, teclistamab-cqyv) Johnson & Johnson·BCMA × CD3 132 trials·t½ ~2–3 weeks at steady state | linvoseltamab (Lynozyfic, REGN5458, linvoseltamab-gcpt) Regeneron·BCMA × CD3 24 trials·t½ IgG-like, supporting weekly then less frequent dosing |
|---|---|---|---|
Overview Program | Carvykti (ciltacabtagene autoleucel) | Tecvayli (teclistamab) | Lynozyfic (linvoseltamab) |
Overview Company | Johnson & Johnson / Legend Biotech | Johnson & Johnson | Regeneron |
Overview Modality | CGT | ANTIBODY | ANTIBODY |
Overview Target | BCMA | BCMA × CD3 | BCMA × CD3 |
Overview Indication | Relapsed or refractory multiple myeloma | Relapsed or refractory multiple myeloma | Relapsed or refractory multiple myeloma after ≥4 prior lines including a PI, an IMiD, and an anti-CD38 antibody |
Overview Phase | APPROVED | APPROVED | APPROVED |
Overview Status | APPROVED | APPROVED | APPROVED |
Overview Content status | Curated Core | Curated Core | Curated Core |
Overview Data Confidence | Data Confidence · High | Data Confidence · High | Data Confidence · High |
Overview Development Signal | Development Signal · Established | Development Signal · Established | Development Signal · Established |
Overview Approval status | FDA approved | FDA approved | FDA approved |
Positioning Key differentiator | Dual-epitope BCMA binding raises avidity and appears to sustain CAR-T persistence longer than single-domain designs. | No manufacturing slot needed, so it can be started immediately in rapidly progressing myeloma. | Response-adapted schedule can stretch to q4w after a deep response, so the compare with Tecvayli is visit burden and CRS step-up, not the antigen. |
Positioning Known limitation | BCMA loss or biallelic deletion, soluble BCMA shedding, T-cell exhaustion, and immunosuppressive marrow niche. | BCMA loss, soluble BCMA acting as a sink, and T-cell exhaustion. | BCMA loss or mutation, T-cell exhaustion, and prior BCMA-directed therapy. |
Positioning Development positioning | Best-in-class efficacy in BCMA CAR-T, ahead of Abecma on depth of response. | Class-defining BCMA engager; competes with Elrexfio and BCMA CAR-T. | Second approved BCMA engager after Tecvayli; dosing frequency is the operational split. |
Technology Vector | Lentiviral | — | — |
MoA Mechanism | Autologous T cells engineered with a dual-epitope BCMA CAR recognize BCMA on malignant plasma cells and trigger MHC-independent cytolysis and clonal CAR-T expansion. | Simultaneously engages BCMA on plasma cells and CD3 on T cells, forming an immune synapse that redirects polyclonal T cells to lyse BCMA+ myeloma cells independent of TCR specificity. | Binds BCMA on myeloma cells and CD3 on T cells, forming a cytolytic synapse that kills the plasma cell independent of native TCR specificity. |
MoA Biomarker | BCMA expression, MRD negativity at 10⁻⁵, CAR transgene persistence. | BCMA expression, MRD negativity, serum free light chain response. | BCMA expression is not a companion diagnostic; soluble BCMA is exploratory. |
PK/PD Half-life | Cellular expansion kinetics rather than classical half-life | ~2–3 weeks at steady state | IgG-like, supporting weekly then less frequent dosing |
PK/PD Species | Peak CAR transgene level, MRD negativity, soluble BCMA decline | Cynomolgus monkey, T-cell activation markers, cytokine profile, soluble BCMA | ORR, MRD, soluble BCMA |
PK/PD Animal (cat.) | Human | Human, NHP | Human |
PK/PD Experiment | PK | pharmacokinetic | — |
Toxicology Species | — | Mouse | — |
Toxicology Major finding | Boxed warnings for CRS, ICANS, parkinsonism and Guillain-Barré syndrome, HLH/MAS, prolonged cytopenia, and secondary T-cell malignancy. | Boxed warning for CRS and neurologic toxicity including ICANS. Profound hypogammaglobulinemia and infection — including opportunistic infection — drive most late morbidity. | Boxed warning for CRS and neurologic toxicity including ICANS. Neutropenia, infection, and hypogammaglobulinemia dominate later cycles. |
Toxicology CRS | CRS in ~95% of CARTITUDE-1 patients, grade ≥3 ~4% | CRS ~72%, grade ≥3 ~0.6% | CRS common, mostly grade 1–2 with step-up |
Clinical Safety signal | Boxed warnings for CRS, ICANS, parkinsonism and Guillain-Barré syndrome, HLH/MAS, prolonged cytopenia, and secondary T-cell malignancy. | Boxed warning for CRS and neurologic toxicity including ICANS. Profound hypogammaglobulinemia and infection — including opportunistic infection — drive most late morbidity. | Boxed warning for CRS and neurologic toxicity including ICANS. Neutropenia, infection, and hypogammaglobulinemia dominate later cycles. |
Clinical Selected reported efficacy | ORR 97% | ORR 63% | ORR 70% |
Clinical Reported ORR | 97% | 63.0% | 70% |
Clinical Reported PFS | HR 0.26 vs standard care in CARTITUDE-4 | ~11.3 mo | — |
Clinical Reported OS | NA | — | — |
Clinical Result source | CARTITUDE-1 (NCT03548207) / CARTITUDE-4 (NCT04181827) | MajesTEC-1 (NCT03145181 / NCT04557098) | LINKER-MM1 (NCT03761108) |
Clinical Program phase | APPROVED | APPROVED | APPROVED |
Clinical Trial activity | No active/completed counts | No active/completed counts | — |
Clinical Trial ref | NCT03548207 | NCT03145181 | NCT03761108 |
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