AZD1981 is a potent, selective CRTh2 (DP2) receptor antagonist with IC50 of 4 nM, showing >1000-fold selectivity over more than 340 other enzymes and receptors, including DP1

>98%

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

AZD-1981; AZD 1981

Powder

DMSO Solubility: 11 mg/mL (28.28 mM)

CRTh2 (DP2) receptor

AZD1981, as a potent antagonist in a disease relevant cell system, inhibits DK-PGD2-induced CD11b expression in human eosinophils with IC50 of 10 nM. AZD1981 blocks DP2-mediated shape change in human eosinophils and basophils in blood, as well as DP2-mediated chemotaxis of human Th2 cells and eosinophils. Moreover, AZD1981 also blocks the binding of PGD2 to mouse, rat, guinea pig, rabbit and dog recombinant DP2.

AZD1981 has high oral bioavailability in male sprague dawley rats. In guinea pig hind limb model, AZD1981 (100 nM) completely inhibits DK-PGD2-induced eosinophil mobilization.

Vistusertib (AZD2014) is an ATP competitive mTOR inhibitor with an IC50 of 2.81 nM. AZD2014 inhibits both mTORC1 and mTORC2 complexes.

>98%

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

AZD2014

Light Yellow Solid

DMSO : ≥ 50 mg/mL (108.10 mM)

mTOR ,P-Akt (S473) ,pS6 (S235/236)

AZD2014 is a close analogue of AZD8055 and a selective inhibitor of mTOR kinase. AZD2014 has greater inhibitory activity against mTORC1 compared to rapamycin: AZD2014 decreases p4EBP1 Thr37/46, inhibits the translation initiation complex and decreases overall protein synthesis while rapamycin has no effect. AZD2014 also inhibits the mTORC2 biomarkers pAKTSer473 and pNDRG1Thr346. AZD2014 has broad antiproliferative activity across multiple tumour cell lines. In particular, AZD2014 induces growth inhibition and cell death in breast cancer cell lines, including ER+ cell lines with acquired resistance to hormone therapy.

AZD2014 induces tumour growth inhibition against several xenograft models including a human primary explant model of ER+ breast cancer refractory to tamoxifen. The antitumour activity is associated with modulation of both mTORC1 and mTORC2 substrates.

AZD1208 is orally available, small molecule inhibitor of PIM kinases with potential antineoplastic activity.

＞98%

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

AZD-1208；AZD1208；AZD 1208.

Light yellow to yellow Powder

DMSO : 28.5 mg/mL (75.10 mM; Need ultrasonic and warming)

Pim1；Pim3；Pim2

AZD1208 is an orally available, potent and highly selective Pim inhibitor that effectively inhibits all three isoforms. AZD1208 inhibits the growth of several AML cell lines and sensitivity correlates with the level of Pim-1 expression, STAT5 activation and presence of protein tyrosine kinase mutation. AZD1208 causes cell cycle arrest and apoptosis in MOLM-16 cells in culture. This is accompanied by a dose-dependent reduction in phosphorylation of BAD, 4EBP1 and p70S6K. In addition, AZD1208 leads to potent inhibition of colony growth of primary AML cells from bone marrow aspirates and downregulates phosphorylation of Pim targets.

AZD1208 suppresses the growth of MOLM-16 and KG-1a xenograft tumors in vivo in a dose proportional manner.

AZD3229 is a potent pan-KIT mutant inhibitor for the treatment of gastrointestinal stromal tumors.

98%

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

DMSO : 40 mg/mL (83.42 mM; Need ultrasonic)

KIT.

AZD3229 is a potent, pan-KIT mutant inhibitor with potent single digit nM growth inhibition against a diverse panel of mutant KIT driven Ba/F3 cell lines (GI50=1-50 nM). AZD3229 demonstrates potent single digit nM growth inhibition across a broad cell panel, with good margin to KDR-driven effects. Selectivity over KDR can be rationalised predominantly by the interaction of water molecules with the protein and ligand in the active site and its kinome selectivity is similar to the best of the approved GIST agents.

AZD3229 is a potent, pan-KIT mutant inhibitor with potent single digit nM growth inhibition against a diverse panel of mutant KIT driven Ba/F3 cell lines (GI50=1-50 nM). AZD3229 demonstrates potent single digit nM growth inhibition across a broad cell panel, with good margin to KDR-driven effects. Selectivity over KDR can be rationalised predominantly by the interaction of water molecules with the protein and ligand in the active site and its kinome selectivity is similar to the best of the approved GIST agents.

AZD2461是一种新型PARP抑制剂，作用于Pgp比Olaparib亲和力低。AZD2461作用于Pgp比Olaparib亲和力低。

>98%

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

AZD-2461

Ethanol ：39.5 mg/mL (100 mM)

DMSO ：39.5 mg/mL (100 mM)

PARP

AZD2461 has lower affinity for Pgp than does Olaparib.

AZD2461 has an 80-fold increased Mdr1b expression on Olaparib-resistant KB1P tumor T6-28, without inhibition of Pgp. AZD2461 induces loss of 53BP1 expression in mice with KB1P tumors with short-term treatment. Long-term AZD2461 treatment is well tolerated and doubled the median relapse-free survival.

Loss of 53BP1 causes PARP inhibitor resistance in Brca1-mutated mouse mammary tumors.
Jaspers JE,et al. Cancer Discov. 2013 Jan;3(1):68-81. PMID: 23103855

AZD 9272 is a brain-permeable mGluR5 antagonist for the study of gastroesophageal reflux.

98%

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

DMSO:12.8 mg/mL (45.0 mM)

mGluR5 (rat):2.6±0.3 nM, mGluR5 (human):7.6±1.1 nM

AZD9272 (10 μM) does not diminish the response to 10 μM ATP in the background GHEK cells. Increasing concentrations of AZD9272 causes a decrease in the potency and the maximal response of DHPG.[1] AZD9272 completely reverses the glutamate-stimulated (EC80=80 μM) phosphatidyl inositol hydrolysis in human mGluR5-GHEK cells in a concentration-dependent manner, with IC50 of 26±3 nM (n=21).[1]

AZD 9272 (3 μmol/kg; single intravenous) is eliminated from plasma with terminal half-lives between 2 and 6 h. The terminal half-lives following oral dosing are similar to the half-lives following intravenous dosing. The volume of distribution at steady state is intermediate for AZD9272.[1]
AZD9272 (2.84 mg/kg) causes greater than 80% and typically more than 99% MTEP-appropriate responding up to 20 hours after dose, with a decline to approximately 20% at 24 hours after dose, yielding a t1/2 of 21.93 hours, and causes no systematic effects on response rates. The first-time point at which AZD9272 causes >90% MTEP-appropriate response is at 30 minutes after the dose.[2]