Cat. No.: HY-10344

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AZD 6482

(Synonyms: KIN-193)

22 Cited Publications

Customer Review

Based on 22 publication(s) in Google Scholar

AZD 6482 (KIN-193) is a potent and selective p110β inhibitor with an IC₅₀ of 0.69 nM.

For research use only. We do not sell to patients.

Purity: 99.93%
CAS No.: 1173900-33-8
Formula: C₂₂H₂₄N₄O₄
Molecular Weight:408.45

Storage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year

AZD 6482 Chemical Structure

CAS No.: 1173900-33-8

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Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
- Clinical Trial
Chemical Information
Publications (22)
Solvent & Solubility
- In Vitro
- In Vivo
Protocol
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

AZD 6482 (KIN-193) is a potent and selective p110β inhibitor with an IC₅₀ of 0.69 nM.

IC₅₀ & Target^[1]

PI3Kβ

0.69 nM (IC₅₀)

PI3Kδ

13.6 nM (IC₅₀)

PI3Kγ

47.8 nM (IC₅₀)

PI3Kα

136 nM (IC₅₀)

PI3K-C2β

54.1 nM (IC₅₀)

hVps34

3390 nM (IC₅₀)

DNA-PK

53.7 nM (IC₅₀)

mTOR

3930 nM (IC₅₀)

PI4Kα

8830 nM (IC₅₀)

Autophagy

All PI3K Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
Adipocyte	IC₅₀	4.4 μM Compound: AZD-6482	Toxicity in human adipocytes assessed as inhibition of insulin-induced glucose uptake Toxicity in human adipocytes assessed as inhibition of insulin-induced glucose uptake	[PMID: 23010262]
Platelet	EC₅₀	0.13 μM Compound: Chemical Probe: AZD6482; KIN-193	Inhibition of PI3Kbeta in Beagle dog whole blood assessed as reduction in ADP-induced platelet aggregation preincubated for 5 mins followed by ADP addition and measured for 6 mins by impedance aggregometry Inhibition of PI3Kbeta in Beagle dog whole blood assessed as reduction in ADP-induced platelet aggregation preincubated for 5 mins followed by ADP addition and measured for 6 mins by impedance aggregometry	[PMID: 22906130]
Platelet	IC₅₀	0.12 μM Compound: Chemical Probe: AZD6482; KIN-193	Inhibition of PI3Kbeta in human blood assessed as reduction in whole blood shear-induced platelet adhesion and aggregation by measuring reduction in average size of adhered aggregated measured after 5 mins by cone and plate analyzer technique Inhibition of PI3Kbeta in human blood assessed as reduction in whole blood shear-induced platelet adhesion and aggregation by measuring reduction in average size of adhered aggregated measured after 5 mins by cone and plate analyzer technique	[PMID: 22906130]
Platelet	IC₅₀	0.21 μM Compound: Chemical Probe: AZD6482; KIN-193	Inhibition of PI3Kbeta in human blood assessed as reduction in collagen-induced platelet aggregation preincubated for 5 mins followed by collagen addition and measured for 6 mins by impedance aggregometry Inhibition of PI3Kbeta in human blood assessed as reduction in collagen-induced platelet aggregation preincubated for 5 mins followed by collagen addition and measured for 6 mins by impedance aggregometry	[PMID: 22906130]
Platelet	IC₅₀	0.27 μM Compound: 2, AZD6482	Antiplatelet activity against human platelet assessed as inhibition of ADP-induced whole blood aggregation by light transmission aggregometry Antiplatelet activity against human platelet assessed as inhibition of ADP-induced whole blood aggregation by light transmission aggregometry	[PMID: 25042253]
Platelet	IC₅₀	0.27 μM Compound: Chemical Probe: AZD6482; KIN-193	Inhibition of PI3Kbeta in human blood assessed as reduction in ADP-induced platelet aggregation preincubated for 5 mins followed by ADP addition and measured for 6 mins by impedance aggregometry Inhibition of PI3Kbeta in human blood assessed as reduction in ADP-induced platelet aggregation preincubated for 5 mins followed by ADP addition and measured for 6 mins by impedance aggregometry	[PMID: 22906130]
Platelet	IC₅₀	1.4 μM Compound: 2, AZD6482	Antiplatelet activity against dog platelet assessed as inhibition of ADP-induced whole blood aggregation by light transmission aggregometry Antiplatelet activity against dog platelet assessed as inhibition of ADP-induced whole blood aggregation by light transmission aggregometry	[PMID: 25042253]
Platelet	IC₅₀	1.4 μM Compound: Chemical Probe: AZD6482; KIN-193	Inhibition of PI3Kbeta in dog blood assessed as reduction in ADP-induced platelet aggregation preincubated for 5 mins followed by ADP addition and measured for 6 mins by impedance aggregometry Inhibition of PI3Kbeta in dog blood assessed as reduction in ADP-induced platelet aggregation preincubated for 5 mins followed by ADP addition and measured for 6 mins by impedance aggregometry	[PMID: 22906130]
Platelet	IC₅₀	1.8 μM Compound: Chemical Probe: AZD6482; KIN-193	Inhibition of PI3Kbeta in rat blood assessed as reduction in ADP-induced platelet aggregation preincubated for 5 mins followed by ADP addition and measured for 6 mins by impedance aggregometry Inhibition of PI3Kbeta in rat blood assessed as reduction in ADP-induced platelet aggregation preincubated for 5 mins followed by ADP addition and measured for 6 mins by impedance aggregometry	[PMID: 22906130]
Platelet	IC₅₀	280 nM Compound: 2, AZD6482	Antiplatelet activity against human platelet assessed as inhibition of collagen-induced platelet rich plasma aggregation by light transmission aggregometry Antiplatelet activity against human platelet assessed as inhibition of collagen-induced platelet rich plasma aggregation by light transmission aggregometry	[PMID: 25042253]

In Vitro

An in vitrokinase assay demonstrates that AZD 6482 (KIN-193) is highly potent in the inhibition of p110β’s kinase activity (IC₅₀ of 0.69 nM) and has 200, 20, and 70-fold selectivity over p110α, p110δ, and p110γ isoforms, respectively. AZD 6482 also exhibits selectivity of ~80 fold over PI3K-C2β and DNA-PK and more than 1,000-fold over other phosphatidylinositol-3 kinase–related kinases (PIKKs). An inhibitor-kinase interaction profiling of AZD 6482 against a panel of 433 kinases using the KinomeScan approach demonstrates that AZD 6482 is highly selective in its interaction with PI3Ks. To determine whether AZD 6482 selectively targets PTEN-deficient tumors, the effect of AZD 6482 is tested on cell proliferation on a large panel of 422 cancer cell lines using high-throughput tumor cell line profiling. 35% of cell lines with PTEN mutations (20 out of 57) and 16% of cell lines with wild-type PTEN (58 out of 365) are sensitive to AZD 6482 with a threshold of EC₅₀<5 μM^[1].

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

In Vivo

To determine the pharmacodynamics of AZD 6482 (KIN-193) in tumors in vivo, rat fibroblast (Rat1) cells are engineered to express both p53DD, a dominant negative mutant of p53, and a constitutively activated myr-p110β (Rat1-CA-p110β) to enable these cells to form xenograft tumors in mice. For comparison, an isogenic Rat1 cell line expressing p53DD and myr-p110α (Rat1-CA-p110α) is also generated. Rat1-CA-p110α and Rat1-CA-p110β cells are introduced subcutaneously into the contralateral flanks of athymic mice such that tumors driven by activated p110α or p110β would be exposed to identical conditions and that concern about animal-to-animal variability could be eliminated. When tumors reach a volume of ~500 mm³, the tumor-bearing mice receives a single IP injection of AZD 6482 (10 mg/kg). The plasma concentration of AZD 6482 is highest at 1 hour post-injection and declined to undetectable levels by 4h. Concentrations of AZD 6482 in both the CA-p110α- and CA-p110β-driven tumors parallel the plasma concentrations. Analyses of tumor lysates harvested at various time points after AZD 6482 injection reveal that the phosphorylation of AKT is significantly reduced at 1hour after AZD 6482 injection in Rat1-CA-p110β tumors, but remain unchanged in Rat1-CAp110α tumors^[1].

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

Clinical Trial

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991	Plexxikon\|		2011-05	PHASE1

Chemical Information

CAS No. 1173900-33-8
Appearance Solid
Molecular Weight 408.45
Formula C₂₂H₂₄N₄O₄
Color White to light yellow
SMILES

O=C1N2C(C([C@H](NC3=CC=CC=C3C(O)=O)C)=CC(C)=C2)=NC(N4CCOCC4)=C1
Synonyms

KIN-193
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	2 years
	-20°C	1 year

Publications (22)

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Journal Impact Factor

Science

The target landscape of clinical kinase drugs. [Abstract]

2017 Dec 1;358(6367):eaan4368. PMID: 29191878
Cancer Discov

Functional characterization of an isoform-selective inhibitor of PI3K-p110β as a potential anticancer agent. [Abstract]

2012 May;2(5):425-33. PMID: 22588880

AZD 6482 purchased from MedChemExpress. Usage Cited in: Cancer Discov. 2012 May;2(5):425-33. [Abstract]

Effects of KIN-193, GDC-0941, PIK-75 and IC87114 on AKT phosphorylation in PTEN-deficient cell lines as indicated. Representative western blots are shown. Bar graphs represent mean ± SD of western blot quantitations of AKTT308 (n=3).
Nat Commun

Human iPSC-based Modeling of Pulmonary Fibrosis Reveals p300/CBP Inhibition Suppresses Alveolar Transitional Cell State. [Abstract]

2026 Feb 12;17(1):1214. PMID: 41680175
Nat Commun

A PI3K p110β-Rac signalling loop mediates Pten-loss-induced perturbation of haematopoiesis and leukaemogenesis. [Abstract]

2015 Oct 7;6:8501. PMID: 26442967

AZD 6482 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2015 Oct 7;6:8501. [Abstract]

Western blot analysis of Akt signalling in whole BM cells at 7 DPI. Freshly isolated BM cells are treated with DMSO, BYL719, KIN193, GS1101 or NVSPI35 at the 1-μM dose for 2 h (n=6) for each treatment.
Sci Transl Med

PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. [Abstract]

2018 Jul 18;10(450):eaaq1093. PMID: 30021885
Cell Discov

NTRK2 activation cooperates with PTEN deficiency in T-ALL through activation of both the PI3K-AKT and JAK-STAT3 pathways. [Abstract]

2016 Sep 20:2:16030. PMID: 27672444

AZD 6482 purchased from MedChemExpress. Usage Cited in: Cell Discov. 2016 Sep 20:2:16030. [Abstract]

Effects of combined inhibition of PI3K and STAT3 pathways on PTEN-mutated T-ALL cells. (a) Short-term treatment of Ba/F3-shPTEN-NTRK2-Tel cells with isoform-selective inhibitors and Pan-PI3K inhibitor GDC-0032. Cells are treated with DMSO, BYL719, KIN193, GS-1101, GDC-0032 (1 μM) or JAK–STAT inhibitor AZD-1480 (1 μM) for 3 h (n=3) for each treatment. (b) Immunoblot analysis of P-Akt and p-S6 in PF382 and JURKAT cells. Cells are treated with the same inhibitors as in a. (c) Combination of siNTRK2
Cancer Lett

Inhibition of BTF3 sensitizes luminal breast cancer cells to PI3Kα inhibition through the transcriptional regulation of ERα. [Abstract]

2019 Jan:440-441:54-63. PMID: 30315845

AZD 6482 purchased from MedChemExpress. Usage Cited in: Cancer Lett. 2019 Jan:440-441:54-63. [Abstract]

The cells are transfected with either the negative control (siNC) or BTF3 siRNA for 12 hours followed by BKM-120 or AZD-6482 treatment for 48 hours. The protein abundance is determined by an immunoblotting analysis.
Cell Death Dis

CD44/HA signaling mediates acquired resistance to a PI3Kα inhibitor. [Abstract]

2020 Oct 6;11(10):831. PMID: 33024087
Proc Natl Acad Sci U S A

PI3K isoform dependence of PTEN-deficient tumors can be altered by the genetic context. [Abstract]

2014 Apr 29;111(17):6395-400. PMID: 24737887
Cell Syst

Torin2 Exploits Replication and Checkpoint Vulnerabilities to Cause Death of PI3K-Activated Triple-Negative Breast Cancer Cells. [Abstract]

2020 Jan 22;10(1):66-81.e11. PMID: 31812693
Oncogene

PI3K-p110α mediates resistance to HER2-targeted therapy in HER2+, PTEN-deficient breast cancers. [Abstract]

2016 Jul 7;35(27):3607-12. PMID: 26500061

AZD 6482 purchased from MedChemExpress. Usage Cited in: Oncogene. 2016 Jul 7;35(27):3607-12. [Abstract]

(A) Immunoblot analyses in HCC1569 cells treated with BYL719, KIN193 (MedChemexpress) or BKM120 (μM). (B, C) Immunoblot analyses in BT474 and BT474-shPTEN cells treated as indicated in (A).
Cell Rep

Divergent Roles of PI3K Isoforms in PTEN-Deficient Glioblastomas. [Abstract]

2020 Sep 29;32(13):108196. PMID: 32997991
J Drug Deliv Sci Technol

2023 Sep, 87, 104783.
Sci Rep

QSAR analysis on a large and diverse set of potent phosphoinositide 3-kinase gamma (PI3Kγ) inhibitors using MLR and ANN methods. [Abstract]

2022 Apr 12;12(1):6090. PMID: 35414065
Sci Rep

The role of the PIK3CA gene in the development and aging of the brain. [Abstract]

2021 Jan 11;11(1):291. PMID: 33431926
Oncol Rep

PI3Kβ inhibitor AZD6482 exerts antiproliferative activity and induces apoptosis in human glioblastoma cells. [Abstract]

2019 Jan;41(1):125-132. PMID: 30542720

AZD 6482 purchased from MedChemExpress. Usage Cited in: Oncol Rep. 2019 Jan;41(1):125-132. [Abstract]

The expression levels of Bcl-2, Bax and related proteins of the PI3K signalling pathway are used to assess the inhibitory effect of AZD6482. Each protein is analysed in triplicate, and a representative experiment is shown.
J Proteome Res

TMTpro-18plex: The Expanded and Complete Set of TMTpro Reagents for Sample Multiplexing. [Abstract]

2021 May 7;20(5):2964-2972. PMID: 33900084
BMC Cancer

Artificial intelligence to guide precision anticancer therapy with multitargeted kinase inhibitors. [Abstract]

2022 Nov 24;22(1):1211. PMID: 36434556
Cancer Res Commun

Cooperative Roles of Class IA PI3K Isoforms in Translocation-Related Sarcoma Cell Survival and Proliferation. [Abstract]

2026 Apr 1;6(4):976-993. PMID: 41916029
bioRxiv

2026 Jan 18.
bioRxiv

Loss of the tumor suppressor PTEN activates cell-intrinsic interferon signaling to drive immune resistance. [Abstract]

2025 Sep 20:2025.09.17.676669. PMID: 41000885
Tumour Biol

Addition of the p110α inhibitor BYL719 overcomes targeted therapy resistance in cells from Her2-positive-PTEN-loss breast cancer. [Abstract]

2016 Nov;37(11):14831-14839. PMID: 27639383

AZD 6482 purchased from MedChemExpress. Usage Cited in: Tumour Biol. 2016 Nov;37(11):14831-14839. [Abstract]

Western blot analysis of PI3K signaling in NIC-PTEN^L/L cells treated with BYL719, AZD6482, or BKM120.

Solvent & Solubility

In Vitro:

DMSO : 50 mg/mL (122.41 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.4483 mL

12.2414 mL

24.4828 mL

5 mM

0.4897 mL

2.4483 mL

4.8966 mL

10 mM

0.2448 mL

1.2241 mL

2.4483 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Concentration Concentration

Volume Volume

Molecular Weight Molecular Weight

Dilution Calculator

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

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In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.5 mg/mL (6.12 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (6.12 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Protocol

Kinase Assay^[1]

AZD 6482 (KIN-193) is profiled at a concentration of 10 µM against a diverse panel of 433 kinases. Scores for primary screen hits are reported as percent of the DMSO control (% control). For kinases where no score is shown, no measurable binding is detected. The lower the score, the lower the K_d is likely to be, such that scores of zero represent strong hits. Scores are related to the probability of a hit, but are not strictly an affinity measurement. At a screening concentration of 10 µM, a score of less than 10% implies that the false positive probability is less than 20% and the K_d is most likely less than 1 µM. A score between 1-10% implies that the false positive probability is less than 10%, although it is difficult to assign a quantitative affinity from a single-point primary screen. A score of less than 1% implies that the false positive probability is less than 5% and the K_d is most likely less than 1 µM^[1].

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

Cell Assay^[1]

Cell viability is determined. Briefly, cells are seeded in medium containing 5% FBS at a density insuring cell growth throughout drug treatment (~15% for most cell lines). Drug treatment is started 24 h post seeding and continued for 72 h. Cell are fixed and stained using Syto60, a red fluorescent DNA stain. The relative cell number is calculated by taking the ratio of the relative fluorescence intensity from drug treated wells over untreated wells after background subtraction (cells-free wells). Nine doses of AZD 6482 (KIN-193) are used in 2-fold dilution steps ranging from 5.12 µM to 0.02 µM. IC₅₀, corresponding to 50% cell number compared to control (untreated) wells, is determined using a fixed top and bottom sigmoidal fitting algorithm implemented in PipelinePilot^[1].

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

Animal Administration^[1]

Mice^[1]
Approximately 6-8 week-old female nude mice are injected s.c. with Rat1-Myr-HA-p110α(Rat1-CAp110α) cells (1×10⁶ cells in 40% matrigel) in one flank (site 1) and Rat1-Myr-HA-p110β (Rat1-CAp110β) cells (0.5×10⁶ cells in 10% matrigel) in the contralateral flank (site 2). When tumors grow to ~500 mm³, mice are dosed once by ip injection with AZD 6482 formulated in 7.5% NMP, 40% PEG400, 52.5% dH₂O at 0.1 mL/10g body weight and 10 mg/kg. Tumors are collected at 0, 1, 4, 8, and 24 h following compound administration and blood samples are obtained by direct heart puncture. Serum is separated and stored at -80°C. The drug concentrations in serum and tumor samples are assessed by LC-MS/MS analysis by the DMPK group.

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

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (283 KB)
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

References

[1]. Ni J, et al. Functional characterization of an isoform-selective inhibitor of PI3K-p110β as a potential anticancer agent. Cancer Discov. 2012 May;2(5):425-33. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.4483 mL	12.2414 mL	24.4828 mL	61.2070 mL
	5 mM	0.4897 mL	2.4483 mL	4.8966 mL	12.2414 mL
	10 mM	0.2448 mL	1.2241 mL	2.4483 mL	6.1207 mL
	15 mM	0.1632 mL	0.8161 mL	1.6322 mL	4.0805 mL
	20 mM	0.1224 mL	0.6121 mL	1.2241 mL	3.0604 mL
	25 mM	0.0979 mL	0.4897 mL	0.9793 mL	2.4483 mL
	30 mM	0.0816 mL	0.4080 mL	0.8161 mL	2.0402 mL
	40 mM	0.0612 mL	0.3060 mL	0.6121 mL	1.5302 mL
	50 mM	0.0490 mL	0.2448 mL	0.4897 mL	1.2241 mL
	60 mM	0.0408 mL	0.2040 mL	0.4080 mL	1.0201 mL
	80 mM	0.0306 mL	0.1530 mL	0.3060 mL	0.7651 mL
	100 mM	0.0245 mL	0.1224 mL	0.2448 mL	0.6121 mL

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AZD 6482

Kinase Inhibitor Library

PI3K/Akt/mTOR Compound Library

Stem Cell Signaling Compound Library

Anti-Cancer Compound Library

Clinical Compound Library

Autophagy Compound Library

Anti-Aging Compound Library

Differentiation Inducing Compound Library

Oxygen Sensing Compound Library

Glycolysis Compound Library

Cytoskeleton Compound Library

Chemical Probe Library

Anti-Breast Cancer Compound Library

Anti-Lung Cancer Compound Library

Anti-Pancreatic Cancer Compound Library

Anti-Blood Cancer Compound Library

Anti-Cancer Metabolism Compound Library

Anti-Obesity Compound Library

Angiogenesis-Related Compound Library

Glucose Metabolism Compound Library

Anti-Liver Cancer Compound Library

Anti-Colorectal Cancer Compound Library

Anti-Prostate Cancer Compound Library

Anti-Pulmonary Fibrosis Compound Library

Cancer Stem Cells Compound Library

Pain-Related Compound Library

Membrane Protein-targeted Compound Library

Highly Selective Inhibitors Library

Highly Selective Activators Library

Cell Death Library

Anti-Hematopathy Compound Library

Anti-Ovarian Cancer Compound Library

Multi-Target Compound Library

Bioactive Compound Library Max

MCE Bioactive Compound Library

Clinical Compound Library Plus

Bioactive Compound Library

Anti-Fibrosis Compound Library

Anti-Brain Cancer Compound Library

Cell Proliferation Compound Library

High-Throughput Bioactive Compound Library

Anti-Rheumatic Arthritis Compound Library

Posttranslational Modification Library

RNA Binding Bioactive Compound Library

Lactylation Compound Library

Publications Citing Use of MedChemExpress (MCE) AZD 6482

All PI3K Isoforms

Biological Activity

Chemical Information

Publications (22)

Solvent & Solubility

Protocol

Purity & Documentation

References

Help & FAQs

Complete Stock Solution Preparation Table

AZD 6482 Related Classifications

Cat. No.: HY-10344