dTAG-47

dTAG-47 (1-1000 nM; 48 h) dose-dependently inhibits NL-FKBP-Cas9-mediated eGFP disruption in U2OS.eGFP.PEST cells, eliminating activity at 100 nM^[1].
dTAG-47 (0-3000 nM; 48 h) dose-dependently reduces NL-FKBP-Cas9-mediated HDR activity in HEK293T CRBN^+/+ cells, with no effect in CRBN^−/− cells, demonstrating CRBN-dependent Cas9 degradation^[1].
dTAG-47 (0-1000 nM; 48 h) dose-dependently inhibits NL-FKBP-Cas9-mediated indel formation in Drosophila S2 cells^[1].
dTAG-47 (1 μM; added at 0.5, 1, 2, 4, 8, 12, 24, 48 h post-transfection, with total incubation through 72 h post-transfection) modulates NL-FKBP-Cas9 lifetime to regulate DNA repair, with HDR saturating at 24 h and NHEJ accumulating with prolonged Cas9 activity in HEK293T cells targeted at the RBM20 locus^[1].
dTAG-47 (1 μM; added at 0, 0.5, 1, 2, 4, 8, 12, 24, 48 h post-transfection, with total incubation through 72 h post-transfection) modulates NL-FKBP-Cas9 lifetime, with HDR activity saturating at 24 h of Cas9 activity in HEK293T cells targeted at the GAPDH locus^[1].
dTAG-47 (0-1000 nM; 72 h) dose-dependently enhances the on-target specificity of NL-FKBP-Cas9 targeting EMX1 in HEK293T cells, increasing the on-target/off-target indel ratio^[1].
dTAG-47 (0.1-1 µM; 48 h) treatment of HAP1dTAG-KDM5A cells for 48 h increases transcript levels of ERV3-1, ERVV-2, ERVW, and HERVE, but does not significantly alter ZNF208 or ZNF676 transcript levels^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.