CIDD-8633

CIDD-8633 (4-5.5 μM, 7-10 days) inhibits the long-term clonal formation ability of AsPC1 and MIA-PaCa-2 cells^[1].
CIDD-8633 (4-6 μM, 72 h) significantly reduces the levels of phosphorylated-DDR2 and its downstream effector phospho-ERK in AsPC1 and MIA-PaCa-2 cells^[1].
CIDD-8633 (1.5 μM, 48 h) inhibits the nuclear translocation of the DDR2-ERK signaling pathway and blocks the proliferative signals in AsPC1 and MIA-PaCa-2 cells^[1].
CIDD-8633 (0.1-10 μM, 72 h) significantly reduces the proliferation of MIA-PaCa-2 cells and AsPC-1 with IC₂₅s of 4.0 and 5.5 μM, respectively^[1].
CIDD-8633 (4 μM, 16 h) reduces the migration ability of MIA PaCa-2 cells by inhibiting DDR2^[1].
CIDD-8633 (4-6 μM, 72 h) inhibits the cell cycle progression by blocking the G1/S phase in AsPC1 and MIA-PaCa-2 cells CIDD-8633 (4-6 μM, 72 h) induces apoptosis in AsPC1 and MIA-PaCa-2 cells by activating caspase-3^[1].
CIDD-8633 (6 μM, 48 h) upregulates the genes including CDKN1A, DDIT3, IL-1β, PMAIP1, and CASP4 in AsPC1 and MIA-PaCa-2 cells^[1].
CIDD-8633 (4-10 μM, 72 h) significantly reduces the levels of p-DDR2 and p-ERK, and increases the level of cleaved caspase-3 in AsPC1 and MIA-PaCa-2 cells^[1].

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