预约演示
更新于：2026-03-14
Catadegbrutinib
更新于：2026-03-14
概要
基本信息
药物类型 蛋白水解靶向嵌合体（PROTAC） |
别名 3-tert-butyl-N-{(1R)-1-[4-(6-{6-[4-({1-[4-(2,4-dioxo-1,3-diazinan-1-yl)phenyl]piperidin-4-yl}methyl)piperazin-1-yl]pyridin-3-yl}-7H-pyrrolo[2,3-d]pyrimidin-4-yl)-2-methylphenyl]ethyl}-1,2,4-oxadiazole-5-carboxamide、BTK CDAC、BGB 16673 + [3] |
靶点 |
作用方式 降解剂 |
作用机制 BTK 降解剂(酪氨酸蛋白激酶BTK 降解剂) |
非在研适应症- |
非在研机构- |
权益机构- |
最高研发阶段临床3期 |
首次获批日期- |
最高研发阶段(中国)临床3期 |
特殊审评孤儿药 (美国)、孤儿药 (欧盟)、快速通道 (欧盟)、优先药物（PRIME） (欧盟)、快速通道 (美国) |
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结构/序列
分子式C47H54N12O4 |
InChIKeyZSOLMVZWDSGPDD-SSEXGKCCSA-N |
CAS号2736508-60-2 |
关联
10
项与 Catadegbrutinib 相关的临床试验ACTRN12626000174381
An ALLG open-label multi-centre international phase 2 trial to evaluate the safety and efficacy of two years fixed duration therapy with sonrotoclax in combination with the BGB-16673 and rituximab in patients with treatment naïve or BTKi naïve/intolerant Waldenström Macroglobulinemia (WM).
NCT06973187
A Phase 3, Open-Label, Randomized Study to Evaluate the Safety and Efficacy of BGB-16673 Compared to Pirtobrutinib in Patients With Relapsed/Refractory Chronic Lymphocytic Leukemia or Small Lymphocytic Lymphoma
NCT07005713
A Phase 1b, Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of Multiple- Ascending Doses of BGB-16673 in Patients With Chronic Spontaneous Urticaria
100 项与 Catadegbrutinib 相关的临床结果
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100 项与 Catadegbrutinib 相关的转化医学
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100 项与 Catadegbrutinib 相关的专利（医药）
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8
项与 Catadegbrutinib 相关的文献（医药）2025-09-01Cureus Journal of Medical Science
Invasive Cutaneous Mucormycosis in a Patient With Chronic Lymphocytic Leukemia on Obinutuzumab, Idelalisib, and Bruton Tyrosine Kinase Degrader: A Case Report.
Article
作者: Brown, Claire E ; Morinishi, Chelsea D ; Younes, Ramee
Invasive fungal infections (IFIs) due to Mucorales are a significant infectious complication in patients with hematologic malignancy, contributing to high mortality rates. The emergence of new targeted biologic therapies has introduced additional effects on the innate and humoral immune system, which produce variable risk for IFIs. Timely diagnosis and treatment of invasive mucormycosis can be challenging. We present a case of invasive cutaneous mucormycosis in an elderly man with chronic lymphocytic leukemia (CLL), who was receiving a Bruton tyrosine kinase (BTK)-targeted protein degrader trial drug (BGB-16673), obinutuzumab, a newer anti-CD20 monoclonal therapy, and idelalisib, a phosphoinositide 3-kinase inhibitor. While molecular testing and tissue culture were negative, histopathology was essential to early diagnosis. Clinical cure was achieved with limb amputation, given the extent of disease. This case underscores the necessity of a low index of suspicion for mucormycosis on presentation, critical appraisal of the patient's risk factors, and a multimodal approach to diagnosis.
2025-06-01HEMATOLOGICAL ONCOLOGY
Diagnosis and Management of Waldenstrom's Macroglobulinemia
Review
作者: Castillo, Jorge J. ; Sarosiek, Shayna ; Treon, Steven P.
ABSTRACT:
Waldenström macroglobulinemia (WM) is an IgM secreting lymphoplasmacytic lymphoma. Mutations in MYD88 (95%–97%) and CXCR4 (30%–40%) are common in patients with WM. TP53 is also altered in up to 30% of WM patients, particularly those previously treated. Mutated MYD88 triggers the expression and activation of HCK that drives multiple pro‐survival signaling cascades, including BTK. There are over 40 CXCR4 mutation types in WM. WM patients bearing nonsense CXCR4 variants can present with symptomatic hyperviscosity and show greater resistance to covalent BTK inhibitors (cBTK‐i). The cBTK‐i zanubrutinib shows greater response activity and/or improved progression‐free survival in WM patients with wild‐type MYD88, mutated CXCR4, or altered TP53. New or emerging options for patients progressing on c‐BTKi include pirtobrutinib, BGB‐16673, venetoclax, and sonrotoclax. Combinations of BTK inhibitors with chemoimmunotherapy and BCL2 antagonists have advanced. Algorithms for patients with treatment‐naïve and previously treated WM based on genomics, disease characteristics, and co‐morbidities are discussed.
2025-05-01AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS
Bruton Tyrosine Kinase Degraders
Review
作者: Sabakhtarishvili, Giorgi ; Tabbara, Imad A. ; Bajwa, Omer ; Alshebli, Mouza
Bruton tyrosine kinase (BTK) is a key enzyme involved in B-cell development and signaling, making it a crucial target in the treatment of B-cell malignancies, such as chronic lymphocytic leukemia and non-Hodgkin lymphoma. While BTK inhibitors (BTKi), such as ibrutinib, have been effective, resistance—both intrinsic and acquired—poses a significant challenge, often associated with BTK mutations like C481S. To address this, novel BTK degraders have been developed, leveraging proteolysis-targeting chimeras to selectively degrade both wild-type and mutant BTK forms. This approach offers a promising strategy to overcome BTKi resistance.Agents such as NRX-0492, BGB-16673, NX-5948, NX-2127, HZ-Q1060, ABBV-101, and AC676 have shown significant BTK degradation in preclinical and early clinical trials. NRX-0492 demonstrated over 90% BTK degradation with sustained pharmacodynamic effects, whereas BGB-16673 achieved clinical responses in 67% of patients with relapsed/refractory B-cell malignancies. Similarly, NX-5948 and NX-2127 showed potent BTK degradation, with NX-2127, in addition, targeting immunomodulatory proteins, resulting in partial and stable responses in chronic lymphocytic leukemia and non-Hodgkin lymphoma patients. HZ-Q1060, a preclinical candidate, displayed rapid and sustained BTK degradation in vivo. Early-phase trials of ABBV-101 and AC676 are also showing promising results.These BTK degraders have demonstrated favorable safety profiles, with manageable adverse events, and offer a novel therapeutic avenue for patients with BTKi-resistant malignancies. As clinical trials progress, these degraders hold the potential to significantly enhance treatment outcomes, offering a new frontier in personalized cancer therapy.
432
项与 Catadegbrutinib 相关的新闻（医药）2026-03-11
蛋白降解靶向嵌合体抗体药物偶联物引进/卖出
100 项与 Catadegbrutinib 相关的药物交易
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研发状态
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 慢性淋巴细胞白血病 | 临床3期 | 美国 | 2025-04-10 | |
| 慢性淋巴细胞白血病 | 临床3期 | 日本 | 2025-04-10 | |
| 慢性淋巴细胞白血病 | 临床3期 | 阿根廷 | 2025-04-10 | |
| 慢性淋巴细胞白血病 | 临床3期 | 澳大利亚 | 2025-04-10 | |
| 慢性淋巴细胞白血病 | 临床3期 | 巴西 | 2025-04-10 | |
| 慢性淋巴细胞白血病 | 临床3期 | 加拿大 | 2025-04-10 | |
| 慢性淋巴细胞白血病 | 临床3期 | 捷克 | 2025-04-10 | |
| 慢性淋巴细胞白血病 | 临床3期 | 德国 | 2025-04-10 | |
| 慢性淋巴细胞白血病 | 临床3期 | 意大利 | 2025-04-10 | |
| 慢性淋巴细胞白血病 | 临床3期 | 波兰 | 2025-04-10 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床1/2期 | 42 | 艱製鬱構積積憲夢鬱壓(廠壓糧選積繭餘膚製遞) = 壓蓋憲製淵範壓願壓襯 觸構夢膚選蓋衊憲範簾 (憲鏇觸製鬱憲壓餘齋壓 ) 更多 | 积极 | 2025-12-06 | |||
临床1/2期 | 60 | (FL) | 衊範壓願選餘窪齋鑰糧(壓積艱窪淵繭觸衊襯繭) = 廠壓壓鏇鑰蓋醖築網襯 壓淵鏇獵衊齋構壓鑰襯 (範襯醖鑰鹽壓夢選艱鬱 ) 更多 | 积极 | 2025-12-06 | ||
(MZL) | 衊範壓願選餘窪齋鑰糧(壓積艱窪淵繭觸衊襯繭) = 範製製餘艱廠鹹構願範 壓淵鏇獵衊齋構壓鑰襯 (範襯醖鑰鹽壓夢選艱鬱 ) 更多 | ||||||
临床1/2期 | 67 | 願淵蓋廠膚選鹹窪蓋網(憲願願憲觸遞鹽範衊鏇) = 願鹽積製範糧顧鹽築衊 鹽廠廠網糧願艱選艱衊 (壓網齋鑰製壓齋醖製壓 ) 更多 | 积极 | 2025-12-06 | |||
临床1/2期 | - | 82 | (CLL/SLL, WM, MCL, MZL) | 艱網糧遞鹽構壓齋蓋衊(廠獵顧範積範糧窪構膚) = 積鏇膚餘襯獵製選憲遞 衊淵鏇襯網窪憲鏇鹽鹹 (蓋築網衊鹽齋選艱鑰築 ) 更多 | 积极 | 2025-12-06 | |
(CLL/SLL, WM, MCL, MZL) | 鬱顧壓構遞蓋簾壓衊鏇(憲壓繭繭衊淵選構遞齋) = 醖鹹餘網艱觸選鏇遞獵 蓋夢構觸襯選壓夢齋廠 (製願齋鹽繭築鬱鬱蓋夢 ) 更多 | ||||||
临床3期 | 500 | 鑰齋憲積憲鬱壓築蓋築(淵製糧壓醖鬱鑰鬱積齋) = 鹽廠鬱糧積選獵鬱齋膚 築網醖製顧淵壓範衊衊 (醖鑰襯觸艱艱製壓積淵 ) 更多 | 积极 | 2025-12-06 | |||
临床1/2期 | 66 | 選選鬱簾鑰獵構膚顧獵(觸積顧構簾壓觸簾襯獵) = 艱鹽構顧窪壓餘鏇積窪 艱觸淵獵憲積衊壓積範 (壓齋醖鏇繭蓋膚選鑰構 ) 更多 | 积极 | 2025-05-14 | |||
临床1期 | 30 | 醖齋壓觸淵獵製醖鏇鹹(遞窪繭齋觸製淵選觸衊) = 鏇窪憲鬱築餘憲醖餘壓 襯觸蓋遞廠鏇憲鏇膚遞 (範淵範艱顧餘構餘鑰鬱 ) 更多 | 积极 | 2025-05-14 | |||
临床1期 | 49 | 餘築膚齋顧淵製鹽蓋積(願艱鬱網襯鑰鹹糧鏇獵) = 窪艱築艱構網廠鹽構鹽 製齋憲齋範鹽觸淵鏇製 (蓋鑰繭築艱選簾鏇鑰夢 ) 更多 | 积极 | 2024-12-09 | |||
N/A | - | 淵觸範鑰築製鹹糧糧膚(鹽構夢憲鹽襯製鏇願選) = No DLTs occurred, and the MTD was not reached 蓋願夢蓋鹽積簾鬱醖積 (夢範艱憲衊獵鹽顧窪齋 ) 更多 | - | 2024-12-09 | |||
BGB-16673 200 mg | |||||||
N/A | - | 淵願窪製築鬱憲齋願衊(餘襯壓遞獵積衊醖鏇蓋) = No DLTs occurred and the MTD was not reached 選夢壓鏇夢繭醖範蓋製 (夢簾餘艱淵選壓繭遞觸 ) 更多 | - | 2024-12-07 | |||
BGB-16673 200 mg |
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