MIT-002(MIT-002) - 在研适应症：黄斑变性，肝硬化，肿瘤_专利_临床

概要

基本信息

药物类型

小分子化药

别名

靶点-

作用机制-

治疗领域

肿瘤遗传病与畸形消化系统疾病+ [1]

在研适应症

黄斑变性肝硬化肿瘤+ [1]

非在研适应症-

原研机构

Mitoimmune Therapeutics, Inc.初创企业

在研机构

Mitoimmune Therapeutics, Inc.初创企业

非在研机构-

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-

关联

100 项与 MIT-002 相关的临床结果

登录后查看更多信息

100 项与 MIT-002 相关的转化医学

登录后查看更多信息

100 项与 MIT-002 相关的专利（医药）

登录后查看更多信息

1

项与 MIT-002 相关的文献（医药）

1980-05-01·Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis

Comparison of toxicity and mutagenicity of methylnitrosourea, methylnitronitrosoguanidine and ICR-191 among human lymphoblast lines

Article

作者: William G. Thilly ; Saul A. Slapikoff ; Barbara M. Andon

The toxic and mutagenic effects of the alkylating agents methylnitrosourea (MNU) and methylnitronitrosoguanidine (MNNG) and of the frameshift mutagen, ICR-191 were compared among 3 human diploid lymphoblast lines, MIT-2, WI-L2 and GM 130. The MIT-2 and WI-L2 lines were both sensitive to the toxic and mutagenic effects of all 3 agents tested. The WI-L2 line was more sensitive to the toxic effects of MNU and MNNG than the MIT-2 line, while it was somewhat less sensitive to the mutagenic effects of these alkylating agents. The GM 130 line was strikingly resistant to both the toxic and mutagenic effects of the alkylating agents. The order of sensitivity to the toxic effect of ICR-191 was MIT-2 greater than WI-L2 greater than GM 130, while the order of sensitivity to the mutagenic effects of this frameshift mutagen was GM 130 greater than MIT-2 greater than WI-L2. These results point to the importance of accounting possible variations in mutability among individuals when extrapolating from any single mutagenicity assay for human risk assessment.

100 项与 MIT-002 相关的药物交易

登录后查看更多信息

研发状态

10 条进展最快的记录,

登录

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
黄斑变性	临床前	韩国	Mitoimmune Therapeutics, Inc.初创企业	-
肝硬化	临床前	韩国	Mitoimmune Therapeutics, Inc.初创企业	-
肿瘤	临床前	韩国	Mitoimmune Therapeutics, Inc.初创企业	-
非酒精性脂肪性肝炎	临床前	韩国	Mitoimmune Therapeutics, Inc.初创企业	-