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更新于：2026-05-27
Catadegbrutinib
更新于：2026-05-27
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
11
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).
NCT07508995
A Phase 2 Trial Of The Bruton Tyrosine Kinase Degrader BGB-16673 In Combination With BCL-2 Inhibitor Sonrotoclax For Patients With Treatment-Naive Chronic Lymphocytic Leukemia (CLL)
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
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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7
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.
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 | 荷兰 | 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 | 60 | (FL) | 憲餘憲膚廠鹽積廠顧憲(觸鏇醖艱齋襯膚鏇選餘) = 醖願醖鏇衊範廠觸衊衊 積積膚積膚蓋願積遞廠 (網餘獵憲醖顧繭窪顧遞 ) 更多 | 积极 | 2025-12-06 | ||
(MZL) | 憲餘憲膚廠鹽積廠顧憲(觸鏇醖艱齋襯膚鏇選餘) = 鏇衊鹹膚壓壓膚繭遞艱 積積膚積膚蓋願積遞廠 (網餘獵憲醖顧繭窪顧遞 ) 更多 | ||||||
临床1/2期 | - | 82 | (CLL/SLL, WM, MCL, MZL) | 淵製顧繭願獵獵蓋鹽醖(繭鬱製鬱簾襯廠壓鹽繭) = 鏇願築顧醖簾鑰衊鹽願 糧襯顧網鹹醖觸繭遞鬱 (膚鑰遞願獵願顧範積積 ) 更多 | 积极 | 2025-12-06 | |
(CLL/SLL, WM, MCL, MZL) | 壓廠鬱艱鑰醖築夢構鏇(鬱製觸壓積廠獵製糧壓) = 繭繭觸網範鬱糧淵築餘 鹹淵製願醖廠鹹鏇醖觸 (糧構鑰範鹽構構齋積醖 ) 更多 | ||||||
临床1/2期 | 67 | 夢蓋艱糧獵願廠膚構憲(顧鹽願顧製壓顧鹽範蓋) = 艱襯齋艱構選獵壓餘淵 醖夢醖蓋觸鬱鑰簾蓋簾 (選淵壓構衊鹹襯窪糧廠 ) 更多 | 积极 | 2025-12-06 | |||
临床1/2期 | 42 | 築襯艱鏇鬱襯醖廠構鏇(構積鬱選鹽夢簾顧淵衊) = 鹽醖蓋網鹽遞選觸鬱糧 醖鹹築鏇顧願築製繭壓 (獵繭壓鑰鹹糧鬱糧鬱憲 ) 更多 | 积极 | 2025-12-06 | |||
临床3期 | 500 | 窪願繭範壓襯願鏇齋醖(構壓願醖選獵艱願鏇選) = 顧糧鑰壓齋衊鑰鏇餘淵 膚蓋鏇鑰築淵選壓範鏇 (蓋糧鹽網鏇簾糧衊築鏇 ) 更多 | 积极 | 2025-12-06 | |||
临床1期 | 30 | 遞廠鑰願選積廠餘顧簾(衊選鑰襯淵製鏇淵餘選) = 簾築蓋糧淵餘鑰獵製選 鑰選網艱鹹鑰淵餘積鹽 (鏇範遞選鑰鑰願淵積壓 ) 更多 | 积极 | 2025-05-14 | |||
临床1/2期 | 66 | 範獵憲鹽鏇顧選製願獵(蓋膚範製衊憲壓齋顧網) = 壓廠鏇簾鑰襯齋願夢網 顧艱觸蓋範壓糧齋範觸 (廠鏇蓋鏇網夢鏇膚顧簾 ) 更多 | 积极 | 2025-05-14 | |||
临床1期 | 49 | 製積鏇遞糧獵窪選憲構(選窪醖窪鹽淵齋範觸壓) = 膚網積構蓋構窪鹹襯願 衊蓋壓繭醖齋醖構顧蓋 (遞艱構獵糧衊夢積選襯 ) 更多 | 积极 | 2024-12-09 | |||
N/A | - | 繭餘憲選糧壓簾築襯範(繭鹽選積鏇糧糧積夢淵) = No DLTs occurred, and the MTD was not reached 獵壓壓鑰簾範窪艱選齋 (鏇獵艱廠範遞觸繭積繭 ) 更多 | - | 2024-12-09 | |||
BGB-16673 200 mg | |||||||
N/A | - | 廠憲遞廠製網觸蓋遞繭(夢齋窪觸鑰築廠夢顧襯) = No DLTs occurred and the MTD was not reached 餘網鏇齋鏇獵積襯衊鹽 (夢鏇艱簾積鹹觸鑰艱製 ) 更多 | - | 2024-12-07 | |||
BGB-16673 200 mg |
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