Fulvoplumierin(I)分别在四氢-富伏普卢林素(XXIII),六氢-富伏普卢林素(IV),异六氢-富伏普卢林素(XIX)和dasölige,NHHTEinheitlicheüübergberg(fulvo)中 Die Konstitution的死者Stoffe wurdeaufgeklärt。Ausgehend von IV和XXIII位于Struktur I des 5'-Carbomethoxy-3',4';1,2-cumalino-ω-丙烯基-fulvensableiten。
A method of determining the susceptibility of a cancer in a subject to treatment with an antimetabolite includes obtaining a sample of cancer cells from the subject, measuring the level of UDG expression in the cancer cells, and comparing the measured levels of UDG expression in the cancer cells to a control level.
Alkylating agent combinations in the treatment of cancer
申请人:Gerson L. Stanton
公开号:US20060241186A1
公开(公告)日:2006-10-26
This application provides compositions and methods useful in the treatment of certain cancers. In part, this application is based on the recognition that certain molecules that target abasic lesions or AP sites in DNA improve, augment, or potentiate the chemotherapeutic efficacy of certain anticancer agents.
本申请提供了用于治疗某些癌症的组合物和方法。本申请部分是基于这样一种认识,即某些靶向 DNA 中消融性病变或 AP 位点的分子可以改善、增强或增效某些抗癌剂的化疗效果。
COMBINATIONS OF ANTIFOLATE AGENT AND METHOXYAMINE IN THE TREATMENT OF CANCER
申请人:Tracon Pharmaceuticals, Inc.
公开号:EP2173333A2
公开(公告)日:2010-04-14
ANTIFOLATE AGENT COMBINATIONS IN THE TREATMENT OF CANCER
申请人:Theuer Charles P.
公开号:US20080234298A1
公开(公告)日:2008-09-25
Compositions and methods useful in the treatment of certain cancers. The methods include administering, to a patient receiving an antifolate anticancer agent, methoxyamine administered in an amount sufficient to enhance or increase the effect of the antifolate anticancer agent. In part, this application is based on the recognition that certain molecules that target abasic lesions or AP sites in DNA improve, augment, or potentiate the chemotherapeutic efficacy of certain anticancer agents.
ANTIMETABOLITE AGENT COMBINATIONS IN THE TREATMENT OF CANCER
申请人:LIU LILI
公开号:US20100267657A1
公开(公告)日:2010-10-21
A method treating cancer in a subject comprises administering to the subject a therapeutically effective amount of an antimetabolite agent that induces formation of AP sites in cancer cells of the subjects and an amount AP endonuclease inhibitor effective to potentiate the cytotoxicity of the antimetabolite agent to the cancer cells.