PRT3789 is a selective PROTAC degrader targeting SMARCA2, exhibiting a DC50 of 0.72 nM in HeLa cells for SMARCA2 and 14 nM for SMARCA4. By forming a stable ternary complex with Von Hippel-Lindau (VHL) E3 ligase, PRT3789 facilitates polyubiquitination and subsequent proteasomal degradation of SMARCA2. This compound effectively disrupts the integrity of the SWI/SNF chromatin remodeling complex, leading to the downregulation of oncogenic gene expression, decreased chromatin accessibility, and enhanced expression of genes related to antigen processing and presentation. PRT3789 is applicable in research on SMARCA4-mutated solid tumors, including non-small cell lung cancer, endometrial cancer, and several other malignancies.
PRT3789 is a selective PROTAC degrader targeting SMARCA2, exhibiting a DC50 of 0.72 nM in HeLa cells for SMARCA2 and 14 nM for SMARCA4. By forming a stable ternary complex with Von Hippel-Lindau (VHL) E3 ligase, PRT3789 facilitates polyubiquitination and subsequent proteasomal degradation of SMARCA2. This compound effectively disrupts the integrity of the SWI/SNF chromatin remodeling complex, leading to the downregulation of oncogenic gene expression, decreased chromatin accessibility, and enhanced expression of genes related to antigen processing and presentation. PRT3789 is applicable in research on SMARCA4-mutated solid tumors, including non-small cell lung cancer, endometrial cancer, and several other malignancies.
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