구조모아 (StructureMoa)항암 chemical structure spider web
방문타깃 · 모달리티 · 임상 근거 · 비임상 맥락으로 최대 5개 프로그램을 나란히 비교합니다. · 다음 갱신 D-6 · 마지막 9월 2일
현재 선택: 5개 · 임상 갱신 필요 1개
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 | linvoseltamab (Lynozyfic, REGN5458, linvoseltamab-gcpt) Regeneron·BCMA × CD3 24 trials·t½ IgG-like, supporting weekly then less frequent dosing | 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 | ||
|---|---|---|---|---|---|
Overview Program | Tecvayli (teclistamab) | Lynozyfic (linvoseltamab) | Carvykti (ciltacabtagene autoleucel) | Blenrep (belantamab mafodotin) | V001-BCMA |
Overview Company | Johnson & Johnson | Regeneron | Johnson & Johnson / Legend Biotech | GSK | Cancer Institute and Hospital, Chinese Academy of Medical Sciences |
Overview Modality | ANTIBODY | ANTIBODY | CGT | ADC | CGT |
Overview Target | BCMA × CD3 | BCMA × CD3 | BCMA | BCMA | BCMA |
Overview Indication | Relapsed or refractory multiple myeloma | Relapsed or refractory multiple myeloma after ≥4 prior lines including a PI, an IMiD, and an anti-CD38 antibody | Relapsed or refractory multiple myeloma | Multiple myeloma | Advanced Malignant Tumours |
Overview Phase | APPROVED | APPROVED | APPROVED | APPROVED | PHASE_1 |
Overview Status | APPROVED | APPROVED | APPROVED | DISCONTINUED | RECRUITING |
Overview Content status | Curated Core | Curated Core | Curated Core | Curated Core | Limited Data |
Overview Data Confidence | Data Confidence · High | Data Confidence · High | Data Confidence · High | Data Confidence · High | Data Confidence · Low |
Overview Development Signal | Development Signal · Established | Development Signal · Established | Development Signal · Established | Development Signal · Established | Development Signal · Watch |
Overview Approval status | FDA approved | FDA approved | FDA approved | FDA approved | Investigational |
Positioning Key differentiator | 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. | Dual-epitope BCMA binding raises avidity and appears to sustain CAR-T persistence longer than single-domain designs. | BCMA-targeted ADC with ocular AEs | — |
Positioning Known limitation | BCMA loss, soluble BCMA acting as a sink, and T-cell exhaustion. | BCMA loss or mutation, T-cell exhaustion, and prior BCMA-directed therapy. | BCMA loss or biallelic deletion, soluble BCMA shedding, T-cell exhaustion, and immunosuppressive marrow niche. | 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. | Second approved BCMA engager after Tecvayli; dosing frequency is the operational split. | Best-in-class efficacy in BCMA CAR-T, ahead of Abecma on depth of response. | — | — |
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. | Binds BCMA on myeloma cells and CD3 on T cells, forming a cytolytic synapse that kills the plasma cell independent of native 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. | 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 is not a companion diagnostic; soluble BCMA is exploratory. | BCMA expression, MRD negativity at 10⁻⁵, CAR transgene persistence. | BCMA expression on myeloma cells. | — |
PK/PD Half-life | ~2–3 weeks at steady state | IgG-like, supporting weekly then less frequent dosing | Cellular expansion kinetics rather than classical half-life | 16.8 h | — |
PK/PD Species | Cynomolgus monkey, T-cell activation markers, cytokine profile, soluble BCMA | ORR, MRD, soluble BCMA | Peak CAR transgene level, MRD negativity, soluble BCMA decline | 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 warning for CRS and neurologic toxicity including ICANS. Neutropenia, infection, and hypogammaglobulinemia dominate later cycles. | Boxed warnings for CRS, ICANS, parkinsonism and Guillain-Barré syndrome, HLH/MAS, prolonged cytopenia, and secondary T-cell malignancy. | Ocular toxicity (keratopathy, blurred vision) in majority of patients; thrombocytopenia and infusion reactions. | — |
Toxicology CRS | CRS ~72%, grade ≥3 ~0.6% | CRS common, mostly grade 1–2 with step-up | CRS in ~95% of CARTITUDE-1 patients, grade ≥3 ~4% | — | — |
Clinical Safety signal | 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. | Boxed warnings for CRS, ICANS, parkinsonism and Guillain-Barré syndrome, HLH/MAS, prolonged cytopenia, and secondary T-cell malignancy. | Ocular toxicity (keratopathy, blurred vision) in majority of patients; thrombocytopenia and infusion reactions. | — |
Clinical Selected reported efficacy | ORR 63% | ORR 70% | ORR 97% | ORR 6% | — |
Clinical Reported ORR | 63.0% | 70% | 97% | 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) | LINKER-MM1 (NCT03761108) | CARTITUDE-1 (NCT03548207) / CARTITUDE-4 (NCT04181827) | ClinicalTrials.gov NCT05986682 | — |
Clinical Program phase | APPROVED | APPROVED | APPROVED | APPROVED | PHASE_1 |
Clinical Trial activity | No active/completed counts | — | No active/completed counts | No active/completed counts | — |
Clinical Trial ref | NCT03145181 | NCT03761108 | NCT03548207 | NCT05986682 | — |
타깃 · 모달리티 · 임상 근거 · 비임상 맥락으로 최대 5개 프로그램을 나란히 비교합니다. · 다음 갱신 D-6 · 마지막 9월 2일
현재 선택: 5개 · 임상 갱신 필요 1개
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 | linvoseltamab (Lynozyfic, REGN5458, linvoseltamab-gcpt) Regeneron·BCMA × CD3 24 trials·t½ IgG-like, supporting weekly then less frequent dosing | 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 | ||
|---|---|---|---|---|---|
Overview Program | Tecvayli (teclistamab) | Lynozyfic (linvoseltamab) | Carvykti (ciltacabtagene autoleucel) | Blenrep (belantamab mafodotin) | V001-BCMA |
Overview Company | Johnson & Johnson | Regeneron | Johnson & Johnson / Legend Biotech | GSK | Cancer Institute and Hospital, Chinese Academy of Medical Sciences |
Overview Modality | ANTIBODY | ANTIBODY | CGT | ADC | CGT |
Overview Target | BCMA × CD3 | BCMA × CD3 | BCMA | BCMA | BCMA |
Overview Indication | Relapsed or refractory multiple myeloma | Relapsed or refractory multiple myeloma after ≥4 prior lines including a PI, an IMiD, and an anti-CD38 antibody | Relapsed or refractory multiple myeloma | Multiple myeloma | Advanced Malignant Tumours |
Overview Phase | APPROVED | APPROVED | APPROVED | APPROVED | PHASE_1 |
Overview Status | APPROVED | APPROVED | APPROVED | DISCONTINUED | RECRUITING |
Overview Content status | Curated Core | Curated Core | Curated Core | Curated Core | Limited Data |
Overview Data Confidence | Data Confidence · High | Data Confidence · High | Data Confidence · High | Data Confidence · High | Data Confidence · Low |
Overview Development Signal | Development Signal · Established | Development Signal · Established | Development Signal · Established | Development Signal · Established | Development Signal · Watch |
Overview Approval status | FDA approved | FDA approved | FDA approved | FDA approved | Investigational |
Positioning Key differentiator | 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. | Dual-epitope BCMA binding raises avidity and appears to sustain CAR-T persistence longer than single-domain designs. | BCMA-targeted ADC with ocular AEs | — |
Positioning Known limitation | BCMA loss, soluble BCMA acting as a sink, and T-cell exhaustion. | BCMA loss or mutation, T-cell exhaustion, and prior BCMA-directed therapy. | BCMA loss or biallelic deletion, soluble BCMA shedding, T-cell exhaustion, and immunosuppressive marrow niche. | 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. | Second approved BCMA engager after Tecvayli; dosing frequency is the operational split. | Best-in-class efficacy in BCMA CAR-T, ahead of Abecma on depth of response. | — | — |
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. | Binds BCMA on myeloma cells and CD3 on T cells, forming a cytolytic synapse that kills the plasma cell independent of native 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. | 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 is not a companion diagnostic; soluble BCMA is exploratory. | BCMA expression, MRD negativity at 10⁻⁵, CAR transgene persistence. | BCMA expression on myeloma cells. | — |
PK/PD Half-life | ~2–3 weeks at steady state | IgG-like, supporting weekly then less frequent dosing | Cellular expansion kinetics rather than classical half-life | 16.8 h | — |
PK/PD Species | Cynomolgus monkey, T-cell activation markers, cytokine profile, soluble BCMA | ORR, MRD, soluble BCMA | Peak CAR transgene level, MRD negativity, soluble BCMA decline | 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 warning for CRS and neurologic toxicity including ICANS. Neutropenia, infection, and hypogammaglobulinemia dominate later cycles. | Boxed warnings for CRS, ICANS, parkinsonism and Guillain-Barré syndrome, HLH/MAS, prolonged cytopenia, and secondary T-cell malignancy. | Ocular toxicity (keratopathy, blurred vision) in majority of patients; thrombocytopenia and infusion reactions. | — |
Toxicology CRS | CRS ~72%, grade ≥3 ~0.6% | CRS common, mostly grade 1–2 with step-up | CRS in ~95% of CARTITUDE-1 patients, grade ≥3 ~4% | — | — |
Clinical Safety signal | 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. | Boxed warnings for CRS, ICANS, parkinsonism and Guillain-Barré syndrome, HLH/MAS, prolonged cytopenia, and secondary T-cell malignancy. | Ocular toxicity (keratopathy, blurred vision) in majority of patients; thrombocytopenia and infusion reactions. | — |
Clinical Selected reported efficacy | ORR 63% | ORR 70% | ORR 97% | ORR 6% | — |
Clinical Reported ORR | 63.0% | 70% | 97% | 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) | LINKER-MM1 (NCT03761108) | CARTITUDE-1 (NCT03548207) / CARTITUDE-4 (NCT04181827) | ClinicalTrials.gov NCT05986682 | — |
Clinical Program phase | APPROVED | APPROVED | APPROVED | APPROVED | PHASE_1 |
Clinical Trial activity | No active/completed counts | — | No active/completed counts | No active/completed counts | — |
Clinical Trial ref | NCT03145181 | NCT03761108 | NCT03548207 | NCT05986682 | — |
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