生物活性

Verteporfin was also found to inhibit autophagosome formation that does not require exposure to light. Verteporfin could target and modify p62 directly, a protein of scaffold and adaptor that binds both polyubiquitinated proteins destined for degradation and LC3 on autophagosomal membranes. Co-immunoprecipitation experiments demonstrated that crosslinked p62 oligomers retain their ability to bind to LC3 but show defective binding to polyubiquitinated proteins. Interestingly, small amounts of crosslinked p62 oligomers were detected in cells which were untreated, and other groups which were noted the accumulation of p62 forms with reduced SDS-PAGE mobility in cellular and animal models of oxidative stress and aging.

体外研究

体内研究

激酶实验

细胞实验

动物实验

不同实验动物依据体表面积的等效剂量转换表（数据来源于FDA指南）

例如，已知某工具药用于小鼠的剂量为88 mg/kg , 则用于大鼠的剂量换算方法：将88 mg/kg 乘以小鼠的Km系数（3），再除以大鼠的Km系数（6），得到该药物用于大鼠的等效剂量44 mg/kg。

参考文献

[1] Schmidt-Erfurth U, et al. Surv Ophthalmol, 2000, 45(3), 195-214.
[2] Brodowska et al (2014) The clinically used photosensitizer Verteporfin (VP) inhibits YAP-TEAD and human retinoblastoma cell growth in vitro without light activation. Exp.Eye Res. 124 67.
[3] Song et al (2014) Hippo coactivator YAP1 upregulates SOX9 and endows esophageal cancer cells with stem-like properties. Cancer Res. 74 4170.
[4] Liu-Chittenden et al (2012) Genetic and pharmacological disruption of the TEAD-YAP complex suppresses the oncogenic activity of YAP. Genes Dev. 26 1300.

体内溶解度

Clinical Trial Information ( data from http://clinicaltrials.gov )

注：以上所有数据均来自公开文献，并不保证对所有实验均有效，数据仅供参考。

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