A0233
AS605240
≥98% (HPLC)
Synonym(s):
5-(6-Quinoxalinylmethylene)-2,4-thiazolidinedione
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About This Item
Empirical Formula (Hill Notation):
C12H7N3O2S
CAS Number:
Molecular Weight:
257.27
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
Recommended Products
Quality Level
Assay
≥98% (HPLC)
form
powder
color
, faint red to orange to dark brown
solubility
DMSO: 1 mg/mL, clear (warmed)
storage temp.
2-8°C
SMILES string
O=C1NC(=O)C(\S1)=C\c2ccc3nccnc3c2
InChI
1S/C12H7N3O2S/c16-11-10(18-12(17)15-11)6-7-1-2-8-9(5-7)14-4-3-13-8/h1-6H,(H,15,16,17)/b10-6-
InChI key
SQWZFLMPDUSYGV-POHAHGRESA-N
Application
AS605240 has been used:
- as a phosphatidylinositol 3-kinase (PI3K) inhibitor to study its effect on Rab5-positive early endosome (EE) vesicles.
- as a (PI3K) inhibitor to treat splenocytes for graft-versus-host disease (GVHD) induction.
- as a class 1A PI3K inhibitor to treat CD4+ T cells.
Biochem/physiol Actions
AS605240 inhibits human recombinant phosphatidylinositol 3-kinase (PI3K) γ, α, β, and δ by competing with adenosine triphosphate (ATP). It plays a role in protecting injury following ischemic stroke. AS605240 also inhibits the activation of astrocytes under the influence of Interleukin-6 (IL-6) and its soluble receptor (sIL-6R). It reduces collagen deposition and prevents lung inflammation. AS605240 also inhibits the increase of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) expression instigated by bleomycin. It is effective in preventing pulmonary fibrosis by inhibiting the transforming growth factor β1 (TGF-β1) and T lymphocytes infiltration into lungs.
AS605240 is a potent and selective PI3Kγ inhibitor.
Features and Benefits
This compound is a featured product for Kinase Phosphatase Biology research. Click here to discover more featured Kinase Phosphatase Biology products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound is featured on the Phosphoinositide Kinases page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
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Irene Filippi et al.
Journal of cellular physiology, 229(12), 2067-2076 (2014-05-14)
Hypoxia represents an inadequate oxygen supply to tissues, which can modulate cell functions, primarily through the hypoxia-inducible transcription factor HIF-1α. Dendritic cells (DC) are professional antigen-presenting cells and their migration maybe affected by hypoxia, since the local microenvironment in lymphoid
Cheng-Chang Chen et al.
Cell chemical biology, 24(7), 907-916 (2017-07-22)
To resolve the subcellular distribution of endolysosomal ion channels, we have established a novel experimental approach to selectively patch clamp Rab5 positive early endosomes (EE) versus Rab7/LAMP1-positive late endosomes/lysosomes (LE/LY). To functionally characterize ion channels in endolysosomal membranes with the patch-clamp
Xin Wei et al.
Biochemical and biophysical research communications, 397(2), 311-317 (2010-06-01)
Phosphoinositide 3-kinase-gamma (PI3Kgamma) has been identified to play the critical roles in inflammatory cells activation and recruitment in multiply inflammatory diseases and it promised to be a prospective target for relevant inflammatory diseases therapy. AS605240, a selective PI3Kgamma inhibitor, has
Xinyi Yu et al.
Scientific reports, 8(1), 10988-10988 (2018-07-22)
Chronic kidney disease (CKD) poses a formidable challenge for public healthcare worldwide as vast majority of patients with CKD are also at risk of accelerated cardiovascular disease and death. Renal fibrosis is the common manifestation of CKD that usually leads
André Bortolini Silveira et al.
Oncotarget, 6(15), 13105-13118 (2015-04-15)
The PI3K pathway is frequently hyperactivated in primary T-cell acute lymphoblastic leukemia (T-ALL) cells. Activation of the PI3K pathway has been suggested as one mechanism of glucocorticoid resistance in T-ALL, and patients harboring mutations in the PI3K negative regulator PTEN
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