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更新于：2025-05-07

TAK-632

更新于：2025-05-07

概要

概要

基本信息

药物类型

小分子化药

别名

pan-Raf inhibitor - Takeda

靶点

RIPK1 x RIPK3 x Raf kinase

作用方式

抑制剂

作用机制

RIPK1抑制剂(受体相互作用的丝氨酸/苏氨酸蛋白激酶-1抑制剂)、RIPK3抑制剂(receptor interacting serine/threonine kinase 3 inhibitors)、Raf kinase抑制剂(RAF丝氨酸/苏氨酸蛋白激酶家族抑制剂)

治疗领域

肿瘤皮肤和肌肉骨骼疾病

在研适应症

黑色素瘤

非在研适应症-

原研机构

Takeda Pharmaceutical Co., Ltd.

在研机构

Takeda Pharmaceutical Co., Ltd.

非在研机构-

权益机构-

最高研发阶段临床前

首次获批日期-

最高研发阶段(中国)-

特殊审评-

结构/序列

分子式C27H18F4N4O3S

InChIKeyOJFKUJDRGJSAQB-UHFFFAOYSA-N

CAS号1228591-30-7

关联

100 项与 TAK-632 相关的临床结果

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100 项与 TAK-632 相关的转化医学

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100 项与 TAK-632 相关的专利（医药）

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项与 TAK-632 相关的文献（医药）

2024-12-16·ChemPhysChem

Article

2024-09-01·Cell Reports

Cell-specific models reveal conformation-specific RAF inhibitor combinations that synergistically inhibit ERK signaling in pancreatic cancer cells

Article

作者: Wynne, Kieran ; Dyn’ko, Uscinnia ; Rukhlenko, Oleksii S. ; Rukhlenko, Oleksii S ; Kolch, Walter ; Koubova, Katerina ; Kholodenko, Boris N. ; Rauch, Nora ; Sevrin, Thomas ; Imoto, Hiroaki ; Dyn'ko, Uscinnia ; Robertson, Sarah ; Kholodenko, Boris N

Pancreatic ductal adenocarcinoma (PDAC) presents significant challenges for targeted clinical interventions due to prevalent KRAS mutations, rendering PDAC resistant to RAF and MEK inhibitors (RAFi and MEKi). In addition, responses to targeted therapies vary between patients. Here, we explored the differential sensitivities of PDAC cell lines to RAFi and MEKi and developed an isogenic pair comprising the most sensitive and resistant PDAC cells. To simulate patient- or tumor-specific variations, we constructed cell-line-specific mechanistic models based on protein expression profiling and differential properties of KRAS mutants. These models predicted synergy between two RAFi with different conformation specificity (type I½ and type II RAFi) in inhibiting phospho-ERK (ppERK) and reducing PDAC cell viability. This synergy was experimentally validated across all four studied PDAC cell lines. Our findings underscore the need for combination approaches to inhibit the ERK pathway in PDAC.

2024-03-01·FlatChem

Fabrication of hyaluronic acid with graphene quantum dot as a dual drug delivery system for cancer therapy

作者: Lin, Jung-Hua ; Cho, Er-Chieh ; Lee, Kuen-Chan ; Yeh, Tseng-Yu ; Zheng, Jia-Huei ; Lin, Joseph

With recent advancements in nanomedicine, there has been growing interest in developing drug delivery systems with multifunctional capabilities.In this study, we developed a novel dual drug delivery system by combining two drug carriers via pos. and neg. electrostatic interactions.First, we modified polyethyleneimine (PEI) with graphene quantum dots (GQDs) to create a pos. charged particle (GPI) with high drug loading efficiency and good dispersibility.Second, we embedded the pyrenebutyric acid structure in hyaluronic acid (HA) through EDC/NHS crosslinking and used TAK-632 as the hydrophobic drug to create neg. charged particles (HANPs) with hydrogel-like properties and the CD44 receptor.After the two components were constructed, the increase in the particle charge and simultaneous delivery of both drugs synergistically enhanced the therapeutic effect of this strategy.Qual. tests confirmed the successful synthesis of the drug carrier, while the potential of this system as a cancer treatment strategy was evaluated in HCT116 cancer cells (through MTT cell viability assays) and in vivo mice xenograft experimentsOur results demonstrated that the dual drug delivery system, HANPs(TAK)/GPI(DOX), had a significant inhibitory effect on the growth of cancer cells both in vitro and in vivo, suggesting that this system is a promising candidate for a new type of treatment.

100 项与 TAK-632 相关的药物交易

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