＞98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

PD 0166285; PD-0166285

DMSO : 65 mg/mL (126.85 mM; Need ultrasonic)

Wee1；Myt1；Chk1

PD0166285 is identified to inhibit Wee1 activity at nanomolar concentrations. The inhibitor abrogates G2/M checkpoint inducing early cell division. At the cellular level, 0.5 μM PD0166285 dramatically inhibits irradiation-induced Cdc2 phosphorylation at the Tyr-15 and Thr-14 in seven of seven cancer cell lines tested. This G2 checkpoint abrogation by PD0166285 is demonstrated to kill cancer cells.PD0166285 does not inhibit Cdc2/cyclin B but inhibits Chk1 kinase at a much higher concentration (3433 nM). the treatment of cells with the inhibitor is related to microtubule stabilization and decrease in cyclin D transcription. Thus, PD0166285 may be a potentially useful anti-cancer therapy.

PD0166285 at 0.5 μM concentration can inhibit Cdc2Y15 /T14 phosphorylation in all cell lines tested, regardless of their p53 status and pharmacological targeting of WEE1 by PD0166285 sensitizes U251-FM GBM tumors to IR in vivo.

PD123319是一种有效的，选择性AT2血管紧张素Ⅱ受体拮抗剂， IC50为34 nM。

≥98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

PD123319; PD-123319; (S)-(+)-PD 123319

powder

DMSO ：100 mg/mL (196.61 mM)
Water ：100 mg/mL (196.61 mM)
Ethanol ：100 mg/mL (196.61 mM)

AT2 receptor

PD 123319 is shown to discriminate between two subclasses of AII receptors in many different tissues. 125I-AII specifically labeled two classes of binding sites for AII in a membrane preparation of bovine adrenal glomerulosa cells. The first class (DuP-753 sensitive) represents approximately 85% of the total binding sites for AII and possesses a high affinity (IC50 of 92.9 nM) for DuP-753. PD-123319 does not have any effect on 125I-AII binding to this site. The second class of binding sites is more sensitive to PD-123319, with an IC50 of 6.9 nM, and has a much lower affinity for DuP-753 (IC50 around 10 microM).

PD 123319 has no effect on cerebral blood flow autoregulation. Acute AT2-receptor blockade does not influence CBF autoregulation. Intravenous administration of PD 123319 to conscious hypertensive rats elicites an immediate dose-dependent increase in MAP that is sustained for approximately 7.4 min with 3 mg/kg PD 123319.

A selective ETA endothelin receptor antagonist.

Store at -20° C

Powder

132991

PD0325901 is a selective and non ATP-competitive MEK inhibitor with IC50 of 0.33 nM in cell-free assays, roughly 500-fold more potent than CI-1040 on phosphorylation of ERK1 and ERK2. Phase 2.

>98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

PD 0325901; PD325901; PD-0325901

白色或类白色粉末

DMSO : ≥ 56 mg/mL (116.14 mM)

MEK

PF0325901 shows higher permeability, and should be able to achieve higher systemic exposures than CI-1040. PD0325901 is exquisitely specific and highly potent against purified MEK, revealing a Kiapp of 1 nM against activated MEK1 and MEK2. PD0325901 is roughly 500-fold more potent than CI-1040 with respect to its cellular effects on phosphorylation of ERK1 and ERK2, displaying subnanomolar activity. PD0325901 prevents the growth of melanoma cell lines. PD0325901 inhibits the growth of TPC-1 cells and K2 cells with GC50 of 11 nM and 6.3 nM, respectively. PD0325901 significantly prevents the the growth of PTC cells harboring a BRAF mutation at very low concentration (10 nM) and only moderately increases the growth of the PTC cells carrying the RET/PTC1 rearrangement at the same concentration. PD0325901 effectively inhibits the phosphorylation of ERK1/2 in multiple PTC cell lines.

PD0325901 (25 mg/kg, p.o.) inhibits phosphorylation of ERK by more than 50% at 24 hours post-dosing. The dose required to produce a 70% incidence of complete tumor responses (C26 model) is 25 mg/kg/day versus 900 mg/kg/day for PD0325901 and CI-1040, respectively. Anticancer activity of PD 0325901 has been demonstrated for a broad spectrum of human tumor xenografts. PD0325901 (20-25 mg/kg/day, p.o.) treatment in mice, shows no tumor growth inoculated with PTC cells bearing a BRAF mutation. For PTC with the RET/PTC1 rearrangement, the average tumor volume of the orthotopic tumor is decreased by 58% as compared with controls. PTC cells carrying a BRAF mutation are more sensitive to PD0325901 than are PTC cells carrying the RET/PTC1 rearrangement.