PD 0332991 (Palbociclib) HCl,827022-32-2,IC-0209786

PD 0332991, as an orally active potent and highly selective inhibitor of CDK4 and CDK6 kinases, can block pRb phosphorylation and subsequently inducing G1 arrest in sensitive cell lines in low nanomolar concentrations. [1][2]
In vitro, single treatment with 8 μmol/L or 16 μmol/L gefinitib inhibited PC-9 cell proliferation.[3] In vitro efficacy test it shown that PD-0332991 acted as a concentration-dependent inhibitor of cell proliferation with an IC50 of 0.65 and 0.58 μM, respectively, in HEC1A and HEC108 cells, however, PD-0332991 did not inhibit cell proliferation in ECC and TEN cells, even at concentrations of up to 1 μM.[4] PD-0332991 has G0/G1 cell-cycle arrest, induction of late apoptosis, and blockade of RB phosphorylation in RCC cell lines with IC50 values ranged from 25.0 nM to 700 nM. [5] PD 0332991 inhibited the AN, RY, G401 and NS cell lines with IC50 of 0.01 μM, 0.01 μM, 0.06 μM, and 0.6 μM, respectively. And PD 0332991 at 0 to 1.0 μM concentrations induced G1 arrest in the AN, RY, G401 and NS cell lines in a concentration-dependent manner, but had no effect on YM cells.[6]
In vivo, treatment with 150 mg/kg PD 0332991 and 100 mg/kg gefitinib inhibited tumor growth, all of the mice had a tumor volume < 30 mm3 after 14 days of treatment, and 20% (2/10) of the mice were completely cured without relapse.[3] In vivo, nu/nu BALB/c nude mice with EC109 cells s.c. were treated with 150 mg/kg orally PD‐0332991, the results shown that PD‐0332991 significantly inhibited the growth curve (tumour volume versus time curve) of EC109 tumours. And the tumour weight in the PD‐0332991‐treated mice was obviously lower than the vehicle‐treated mice.[7]