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 | teclistamab (Tecvayli, JNJ-64007957, teclistamab-cqyv) Johnson & Johnson·BCMA × CD3 132 trials·t½ ~2–3 weeks at steady state | 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 | linvoseltamab (Lynozyfic, REGN5458, linvoseltamab-gcpt) Regeneron·BCMA × CD3 24 trials·t½ IgG-like, supporting weekly then less frequent dosing | |
|---|---|---|---|---|
Overview Program | Tecvayli (teclistamab) | Carvykti (ciltacabtagene autoleucel) | Lynozyfic (linvoseltamab) | Blenrep (belantamab mafodotin) |
Overview Company | Johnson & Johnson | Johnson & Johnson / Legend Biotech | Regeneron | GSK |
Overview Modality | ANTIBODY | CGT | ANTIBODY | ADC |
Overview Target | BCMA × CD3 | BCMA | BCMA × CD3 | BCMA |
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 | Multiple myeloma |
Overview Phase | APPROVED | APPROVED | APPROVED | APPROVED |
Overview Status | APPROVED | APPROVED | APPROVED | DISCONTINUED |
Overview Content status | Curated Core | Curated Core | Curated Core | Curated Core |
Overview Data Confidence | Data Confidence · High | Data Confidence · High | Data Confidence · High | Data Confidence · High |
Overview Development Signal | Development Signal · Established | Development Signal · Established | Development Signal · Established | Development Signal · Established |
Overview Approval status | FDA approved | FDA approved | FDA approved | FDA approved |
Positioning Key differentiator | No manufacturing slot needed, so it can be started immediately in rapidly progressing myeloma. | Dual-epitope BCMA binding raises avidity and appears to sustain CAR-T persistence longer than single-domain designs. | 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. | BCMA-targeted ADC with ocular AEs |
Positioning Known limitation | BCMA loss, soluble BCMA acting as a sink, and T-cell exhaustion. | BCMA loss or biallelic deletion, soluble BCMA shedding, T-cell exhaustion, and immunosuppressive marrow niche. | BCMA loss or mutation, T-cell exhaustion, and prior BCMA-directed therapy. | bypass this immune effector cell dependence, we developed a novel strategy using antibody-drug conjugates (ADCs) |
Positioning Development positioning | Class-defining BCMA engager; competes with Elrexfio and BCMA CAR-T. | Best-in-class efficacy in BCMA CAR-T, ahead of Abecma on depth of response. | Second approved BCMA engager after Tecvayli; dosing frequency is the operational split. | — |
Technology Payload | — | — | — | MMAF |
Technology Linker | — | — | — | Non-cleavable |
Technology Vector | — | Lentiviral | — | — |
MoA Mechanism | 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. | 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. | Binds BCMA on myeloma cells and CD3 on T cells, forming a cytolytic synapse that kills the plasma cell independent of native TCR specificity. | Belantamab mafodotin binds BCMA on plasma cells; afucosylated Fc enhances immune engagement while MMAF (microtubule inhibitor) payload is internalized and causes cell death. |
MoA Biomarker | BCMA expression, MRD negativity, serum free light chain response. | BCMA expression, MRD negativity at 10⁻⁵, CAR transgene persistence. | BCMA expression is not a companion diagnostic; soluble BCMA is exploratory. | BCMA expression on myeloma cells. |
PK/PD Half-life | ~2–3 weeks at steady state | Cellular expansion kinetics rather than classical half-life | IgG-like, supporting weekly then less frequent dosing | 16.8 h |
PK/PD Species | Cynomolgus monkey, T-cell activation markers, cytokine profile, soluble BCMA | Peak CAR transgene level, MRD negativity, soluble BCMA decline | ORR, MRD, soluble BCMA | Cynomolgus monkey, Human, M-protein, corneal microcysts on ophthalmic exam |
PK/PD Animal (cat.) | Human, NHP | Human | Human | Human, NHP |
PK/PD Experiment | pharmacokinetic | PK | — | Pd |
Toxicology Species | Mouse | — | — | Cynomolgus monkey, Mouse, Rat, Human |
Toxicology Animal (cat.) | — | — | — | Human |
Toxicology Major finding | Boxed warning for CRS and neurologic toxicity including ICANS. Profound hypogammaglobulinemia and infection — including opportunistic infection — drive most late morbidity. | 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. Neutropenia, infection, and hypogammaglobulinemia dominate later cycles. | Ocular toxicity (keratopathy, blurred vision) in majority of patients; thrombocytopenia and infusion reactions. |
Toxicology CRS | CRS ~72%, grade ≥3 ~0.6% | CRS in ~95% of CARTITUDE-1 patients, grade ≥3 ~4% | CRS common, mostly grade 1–2 with step-up | — |
Clinical Safety signal | Boxed warning for CRS and neurologic toxicity including ICANS. Profound hypogammaglobulinemia and infection — including opportunistic infection — drive most late morbidity. | 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. Neutropenia, infection, and hypogammaglobulinemia dominate later cycles. | Ocular toxicity (keratopathy, blurred vision) in majority of patients; thrombocytopenia and infusion reactions. |
Clinical Selected reported efficacy | ORR 63% | ORR 97% | ORR 70% | ORR 6% |
Clinical Reported ORR | 63.0% | 97% | 70% | 6% |
Clinical Reported PFS | ~11.3 mo | HR 0.26 vs standard care in CARTITUDE-4 | — | 8.4 |
Clinical Reported OS | — | NA | — | 19 |
Clinical Result source | MajesTEC-1 (NCT03145181 / NCT04557098) | CARTITUDE-1 (NCT03548207) / CARTITUDE-4 (NCT04181827) | LINKER-MM1 (NCT03761108) | ClinicalTrials.gov NCT05986682 |
Clinical Program phase | APPROVED | APPROVED | APPROVED | APPROVED |
Clinical Trial activity | No active/completed counts | No active/completed counts | — | No active/completed counts |
Clinical Trial ref | NCT03145181 | NCT03548207 | NCT03761108 | NCT05986682 |
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 | teclistamab (Tecvayli, JNJ-64007957, teclistamab-cqyv) Johnson & Johnson·BCMA × CD3 132 trials·t½ ~2–3 weeks at steady state | 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 | linvoseltamab (Lynozyfic, REGN5458, linvoseltamab-gcpt) Regeneron·BCMA × CD3 24 trials·t½ IgG-like, supporting weekly then less frequent dosing | |
|---|---|---|---|---|
Overview Program | Tecvayli (teclistamab) | Carvykti (ciltacabtagene autoleucel) | Lynozyfic (linvoseltamab) | Blenrep (belantamab mafodotin) |
Overview Company | Johnson & Johnson | Johnson & Johnson / Legend Biotech | Regeneron | GSK |
Overview Modality | ANTIBODY | CGT | ANTIBODY | ADC |
Overview Target | BCMA × CD3 | BCMA | BCMA × CD3 | BCMA |
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 | Multiple myeloma |
Overview Phase | APPROVED | APPROVED | APPROVED | APPROVED |
Overview Status | APPROVED | APPROVED | APPROVED | DISCONTINUED |
Overview Content status | Curated Core | Curated Core | Curated Core | Curated Core |
Overview Data Confidence | Data Confidence · High | Data Confidence · High | Data Confidence · High | Data Confidence · High |
Overview Development Signal | Development Signal · Established | Development Signal · Established | Development Signal · Established | Development Signal · Established |
Overview Approval status | FDA approved | FDA approved | FDA approved | FDA approved |
Positioning Key differentiator | No manufacturing slot needed, so it can be started immediately in rapidly progressing myeloma. | Dual-epitope BCMA binding raises avidity and appears to sustain CAR-T persistence longer than single-domain designs. | 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. | BCMA-targeted ADC with ocular AEs |
Positioning Known limitation | BCMA loss, soluble BCMA acting as a sink, and T-cell exhaustion. | BCMA loss or biallelic deletion, soluble BCMA shedding, T-cell exhaustion, and immunosuppressive marrow niche. | BCMA loss or mutation, T-cell exhaustion, and prior BCMA-directed therapy. | bypass this immune effector cell dependence, we developed a novel strategy using antibody-drug conjugates (ADCs) |
Positioning Development positioning | Class-defining BCMA engager; competes with Elrexfio and BCMA CAR-T. | Best-in-class efficacy in BCMA CAR-T, ahead of Abecma on depth of response. | Second approved BCMA engager after Tecvayli; dosing frequency is the operational split. | — |
Technology Payload | — | — | — | MMAF |
Technology Linker | — | — | — | Non-cleavable |
Technology Vector | — | Lentiviral | — | — |
MoA Mechanism | 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. | 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. | Binds BCMA on myeloma cells and CD3 on T cells, forming a cytolytic synapse that kills the plasma cell independent of native TCR specificity. | Belantamab mafodotin binds BCMA on plasma cells; afucosylated Fc enhances immune engagement while MMAF (microtubule inhibitor) payload is internalized and causes cell death. |
MoA Biomarker | BCMA expression, MRD negativity, serum free light chain response. | BCMA expression, MRD negativity at 10⁻⁵, CAR transgene persistence. | BCMA expression is not a companion diagnostic; soluble BCMA is exploratory. | BCMA expression on myeloma cells. |
PK/PD Half-life | ~2–3 weeks at steady state | Cellular expansion kinetics rather than classical half-life | IgG-like, supporting weekly then less frequent dosing | 16.8 h |
PK/PD Species | Cynomolgus monkey, T-cell activation markers, cytokine profile, soluble BCMA | Peak CAR transgene level, MRD negativity, soluble BCMA decline | ORR, MRD, soluble BCMA | Cynomolgus monkey, Human, M-protein, corneal microcysts on ophthalmic exam |
PK/PD Animal (cat.) | Human, NHP | Human | Human | Human, NHP |
PK/PD Experiment | pharmacokinetic | PK | — | Pd |
Toxicology Species | Mouse | — | — | Cynomolgus monkey, Mouse, Rat, Human |
Toxicology Animal (cat.) | — | — | — | Human |
Toxicology Major finding | Boxed warning for CRS and neurologic toxicity including ICANS. Profound hypogammaglobulinemia and infection — including opportunistic infection — drive most late morbidity. | 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. Neutropenia, infection, and hypogammaglobulinemia dominate later cycles. | Ocular toxicity (keratopathy, blurred vision) in majority of patients; thrombocytopenia and infusion reactions. |
Toxicology CRS | CRS ~72%, grade ≥3 ~0.6% | CRS in ~95% of CARTITUDE-1 patients, grade ≥3 ~4% | CRS common, mostly grade 1–2 with step-up | — |
Clinical Safety signal | Boxed warning for CRS and neurologic toxicity including ICANS. Profound hypogammaglobulinemia and infection — including opportunistic infection — drive most late morbidity. | 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. Neutropenia, infection, and hypogammaglobulinemia dominate later cycles. | Ocular toxicity (keratopathy, blurred vision) in majority of patients; thrombocytopenia and infusion reactions. |
Clinical Selected reported efficacy | ORR 63% | ORR 97% | ORR 70% | ORR 6% |
Clinical Reported ORR | 63.0% | 97% | 70% | 6% |
Clinical Reported PFS | ~11.3 mo | HR 0.26 vs standard care in CARTITUDE-4 | — | 8.4 |
Clinical Reported OS | — | NA | — | 19 |
Clinical Result source | MajesTEC-1 (NCT03145181 / NCT04557098) | CARTITUDE-1 (NCT03548207) / CARTITUDE-4 (NCT04181827) | LINKER-MM1 (NCT03761108) | ClinicalTrials.gov NCT05986682 |
Clinical Program phase | APPROVED | APPROVED | APPROVED | APPROVED |
Clinical Trial activity | No active/completed counts | No active/completed counts | — | No active/completed counts |
Clinical Trial ref | NCT03145181 | NCT03548207 | NCT03761108 | NCT05986682 |
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