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LY 294002

Catalog No.: GC15485

LY294002 is the first synthetic PI3Kα, δ and β inhibitor

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LY 294002 Chemical Structure

Cas No.:154447-36-6

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Sample solution is provided at 25 µL, 10mM.

Product has been cited by 11 publications

Product Documents

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Kinase experiment [1]:

Preparation Method

PI3K inhibition by LY294002 was determined in a radiometric assay using purified, recombinant enzymes (class IA and class IB) with 1 µM ATP. The kinase reaction was carried out for 1 h at room temperature (24 ℃) and was terminated by addition of PBS.

Reaction Conditions

10µM, 1 h at room temperature


LY294002 not only binds to class I PI3Ks and other PI3K-related kinases, but also to novel targets unrelated to the PI3K family.

Cell experiment [2]:

Cell lines


Reaction Conditions

10µM/L,incubate for 24 and 48h at 37 ℃, 5% CO2


LY294002 and DNR were able to inhibit the growth of K562 cells and promote apoptosis in time- and concentration-dependent manner (P<0.05), both the cell proliferation-inhibiting rate and apoptosis rate in combination therapy group were higher than that in DNR-monotherapy group (P<0.05). After K562 cells treated by LY294002 combined DNR for 36 h, the cells were statistically significantly reduced in G2/M phase (P<0.05), as compared with control group and DNR group. Compared with DNR group, the cell level of G0/G1 phase raised (P<0.05) and cell level of S phase decreased (P>0.05). Compared with DNR group, the expression of SKP2 and BCL-2 mRNA decreased, and the expression of P27 mRNA increased in the combination therapy group (P<0.05).

Animal experiment [3]:

Animal models

Male Wistar rats, weighting 180~200g

Preparation Method

Rats were randomly separated into four groups (with 10 rats in each group): control group, DOI treated group, DOI treated with tiapride group, DOI treated with LY294002 group. Tourette Syndrome was induced in rats by DOI intraperitoneal injection at dosage of 1 mg/kg, once daily for 21 days continuously.

Dosage form

25µg/kg dissolved in 10% dimethyl sulfoxide,intracerebroventricularly injected


LY294002 treatment significantly relieved Tourette syndrome induced by DOI, 5HT2A/c receptor agonist and reduced PI3K/Akt/NF-κB mediated neuroinflammation.


[1]. Gharbi SI, Zvelebil MJ, et al. Exploring the specificity of the PI3K family inhibitor LY294002. Biochem J. 2007 May 15;404(1):15-21.

[2]. Geng YH, Wu WJ, et al. LY294002 Enhaces Chemosensitivity of K562 Cells to Daunorubicin. Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2020 Feb;28(1):110-118.

[3]. Hongyan L, et al. LY294002, a PI3K inhibitor, attenuates Tourette syndrome in rats. Metab Brain Dis. 2017 Oct;32(5):1619-1625.


LY294002, a well-known PI3K signaling pathway inhibitor, is the first synthetic PI3Kα, δ and β inhibitor with IC50 of 500nM, 570nM and 970nM, respectively. LY294002 is not exclusively selective for the PI3Ks, and could in fact act on other lipid kinases and additional apparently unrelated proteins[1]

When LY294002 was added to NPC cells with different concentrations, levels of phosphorylation (S473) Akt were decreased in treated NPC cells, exhibiting a dose-response effect. LY294002 markedly inhibited NPC CNE-2Z cell growth, proliferation, and induced apoptosis in vitro and in vivo[2]. The PI3k/AKT pathway is constitutively activated in a majority of human pancreatic cancer cell lines and the pathway is a promising target for therapeutic intervention. LY294002 produce apoptosis and antiproliferative effects on pancreatic carcinoma cells in vivo and in vitro[3]

LY294002(1.2 mg/kg) was given together with leptin (60 µg/kg) once daily for 14 days via the intraperitoneal (i.p.) route. The result found that body weight in leptin+LY294002-treated rats decreased significantly and STEH was higher (p < 0.001). Ratio of testicular phosphor-Akt/total Akt was significantly higher in leptin+LY294002-treated rats (p < 0.001). The adverse effects of leptin were prevented by concurrent administration of LY294002, suggest the potential involvement of the PI3K signaling pathway in leptin-induced detrimental effects on spermatozoa[4]

[1]. Gharbi SI, Zvelebil MJ, et al. Exploring the specificity of the PI3K family inhibitor LY294002. Biochem J. 2007 May 15;404(1):15-21.
[2]. Jiang H, Fan D, et al. Phosphatidylinositol 3-kinase inhibitor (LY294002) induces apoptosis of human nasopharyngeal carcinoma in vitro and in vivo. J Exp Clin Cancer Res. 2010 Apr 22;29(1):34.
[3]. Bondar VM, Sweeney-Gotsch B, et al. Inhibition of the phosphatidylinositol 3'-kinase-AKT pathway induces apoptosis in pancreatic carcinoma cells in vitro and in vivo. Mol Cancer Ther. 2002 Oct;1(12):989-97. PMID: 12481421.
[4]. Almabhouh FA, et al. LY294002, a PI3K pathway inhibitor, prevents leptin-induced adverse effects on spermatozoa in Sprague-Dawley rats. Andrologia. 2019 Apr;51(3):e13196.

Chemical Properties

Cas No. 154447-36-6 SDF
Chemical Name 2-morpholin-4-yl-8-phenylchromen-4-one
Canonical SMILES C1COCCN1C2=CC(=O)C3=C(O2)C(=CC=C3)C4=CC=CC=C4
Formula C19H17NO3 M.Wt 307.34
Solubility ≥ 40.37mg/mL in DMSO, ≥ 13.55mg/mL in EtOH Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

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Research Update

LY?294002 enhances the chemosensitivity of liver cancer to oxaliplatin by blocking the PI3K/AKT/HIF?1α pathway

Liver cancer remains one of the leading causes of cancer deaths worldwide. The therapeutic effect of oxaliplatin on liver cancer is often limited by acquired resistance of the cancer cells. Abnormal activation of the PI3K/AKT pathway plays an important role in the acquired resistance of oxaliplatin. The present study investigated the effects of the PI3K inhibitor LY?294002 and AKT inhibitor MK2206 on the chemosensitivity of oxaliplatin?resistant liver cancer cells and the molecular mechanism involved. An oxaliplatin?resistant liver cancer cell line HepG2R was developed. MTT assay, clone formation experiments, flow cytometry and Annexin V?FITC/PI staining were used to determine the proliferation, cycle and apoptosis of HepG2R cells when oxaliplatin was combined with LY?294002 or MK2206 treatment. The effects of LY?294002 and MK?2206 on the abnormal activation of PI3K/AKT pathway and hypoxia inducible factor (HIF)?1α protein level in HepG2R cells were detected using western blotting. The results indicated that the PI3K/AKT pathway is stably activated in HepG2R cells. Compared with the AKT inhibitor MK2206, the PI3K inhibitor LY?294002 more effectively downregulated the phosphorylation levels of p85, p110α, p110β, p110γ and AKT in the PI3K/AKT pathway in HepG2R cells, and more effectively inhibited the proliferation of the cells. LY?294002 enhanced the chemotherapy sensitivity of HepG2R cells to oxaliplatin by inducing G0/G1 phase arrest and increasing the proportion of apoptotic cells. In addition, LY?294002 reduced the level of HIF?1α, which is highly expressed in HepG2R cells. It was concluded that LY?294002 enhanced the chemosensitivity of liver cancer cells to oxaliplatin by inhibiting the PI3K/AKT signaling pathway, which may be related to the inhibition of HIF?1α expression. These findings may have clinical significance for the treatment of oxaliplatin?resistant liver cancer.

LY-294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one] affects calcium signaling in airway smooth muscle cells independently of phosphoinositide 3-kinase inhibition

Phosphoinositide 3-kinase (PI3K) may potentially influence intracellular [Ca(2+)](i) concentration by several mechanisms. We have investigated the effects of phosphoinositide 3-kinase (PI3K) inhibitors wortmannin and LY-294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one] on Ca(2+) signaling in rat airway smooth muscle (ASM) cells using fura-2 and imaging methodology. Wortmannin (1 microM) and LY-294002 (1 and 10 microM) had opposite effects: wortmannin caused a small increase, whereas LY-294002 caused a significant decrease of peak Ca(2+) responses to serotonin (5-HT). LY-294002 (10 microM) diminished 5-HT-induced ASM cell contraction, measured as a change in cell surface area, and inositol phosphate formation, measured by anion exchange chromatography. Thin layer chromatography revealed that the levels of phospholipase C (PLC) substrate phosphatidylinositol 4,5-bisphosphate were not affected. SDS polyacrylamide gel electrophoresis and Western blotting have shown that both wortmannin and LY-294002 inhibited platelet-derived growth factor-induced PI3K activation. However, PI3K activation could not be detected after 5-HT stimulation. The specific casein kinase-2 (CK2) inhibitor 5,6-dichloro-1-beta-d-ribofuranosyl-benzimidazole (10-40 microM) reduced 5-HT-triggered responses to a similar extent as LY-294002. We conclude that LY-294002 modulates Ca(2+) signaling in rat ASM independently of its action on PI3K by acting on, or upstream of, PLC, possibly by inhibiting CK2.

LY 294002 inhibits adenosine receptor activation by a mechanism independent of effects on PI-3 kinase or casein kinase II

Adenosine reduces both evoked and spontaneous calcium-dependent acetylcholine (ACh) release through a mechanism downstream of calcium entry at amphibian motor nerve endings (Silinsky EM. J Physiol 1984; 346: 243-56). LY 294002 (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one), an inhibitor of both phosphoinositide-3 kinase (PI-3 kinase) and casein kinase II, has been reported to increase spontaneous ACh release reflected in miniature endplate potential (MEPP) frequencies independently of intraterminal calcium at the frog neuromuscular junction (Rizzoli SO, Betz WJ. J Neurosci 2002; 22: 10680-9). It has been suggested that the increase in MEPP frequency caused by LY 294002, is mediated through an action on synaptotagmins, vesicle associated calcium sensors believed to trigger synaptic vesicle exocytosis. We thus examined the effects of adenosine on MEPP frequencies and evoked ACh release reflected as endplate potentials (EPPs) in order to determine if the presumed calcium-independent ACh release is affected by adenosine. We also wanted to determine if PI-3 kinase or casein kinase II is involved in mediating or modulating the inhibitory effects of adenosine. To these ends, we examined the effects of adenosine in the presence of LY 294002, wortmannin (a highly selective the PI-3 kinase inhibitor), or DRB (5,6-dichlorobenzimidazole riboside, an inhibitor of casein kinase II). LY 294002 reduced the sensitivity of both MEPP frequencies and the nerve-evoked calcium dependent EPPs to adenosine. The occlusive effects of LY 294002 on the actions of adenosine on MEPPs and EPPs were overcome by increasing adenosine concentration. Neither wortmannin nor DRB had any effect on the sensitivity of the EPPs to adenosine indicating that neither PI-3 kinase nor casein kinase II inhibition mediates the reduction in motor-nerve terminal sensitivity to adenosine produced by LY 294002. The results indicate a competitive relationship between LY 294002 and adenosine at A(1) receptors at the frog neuromuscular junction. This effect is independent of the previously described effects of LY 294002 on the exocytotic process, and is also independent of PI-3 kinase or casein kinase II.

LY-294002-inhibitable PI 3-kinase and regulation of baseline rates of Na(+) transport in A6 epithelia

Blocker-induced noise analysis of epithelial Na(+) channels (ENaCs) was used to investigate how inhibition of an LY-294002-sensitive phosphatidylinositol 3-kinase (PI 3-kinase) alters Na(+) transport in unstimulated and aldosterone-prestimulated A6 epithelia. From baseline Na(+) transport rates (I(Na)) of 4.0 +/- 0.1 (unstimulated) and 9.1 +/- 0.9 microA/cm(2) (aldosterone), 10 microM LY-294002 caused, following a relatively small initial increase of transport, a completely reversible inhibition of transport within 90 min to 33 +/- 6% and 38 +/- 2% of respective baseline values. Initial increases of transport could be attributed to increases of channel open probability (P(o)) within 5 min to 143 +/- 17% (unstimulated) and 142 +/- 10% of control (aldosterone) from baseline P(o) averaging near 0.5. Inhibition of transport was due to much slower decreases of functional channel densities (N(T)) to 28 +/- 4% (unstimulated) and 35 +/- 3% (aldosterone) of control at 90 min. LY-294002 (50 microM) caused larger but completely reversible increases of P(o) (215 +/- 38% of control at 5 min) and more rapid but only slightly larger decreases of N(T). Basolateral exposure to LY-294002 induced no detectable effect on transport, P(o) or N(T). We conclude that an LY-294002-sensitive PI 3-kinase plays an important role in regulation of transport by modulating N(T) and P(o) of ENaCs, but only when presented to apical surfaces of the cells.

LY 294002, an inhibitor of phosphatidylinositol 3-kinase, inhibits GH-mediated expression of the IGF-I gene in rat hepatocytes

The signal transduction pathways that mediate GH-dependent regulation of IGF-I gene expression remain poorly defined. To establish a GH-responsive in vitro model system to study the effect of GH on the expression of the endogenous IGF-I gene, primary hepatocytes from adult male rats were prepared. These cells expressed both the GH receptor and the IGF-I gene, as demonstrated using a ribonuclease protection assay. Western blot analyses using antibodies directed against the phosphorylated forms of the ERKs, signal transducer and activator of transcription-5, and Akt/protein kinase B, a protein kinase that is downstream of PI3K, demonstrated GH-dependent phosphorylation of these signaling molecules. These signaling molecules are components of the major signal transduction pathways that are activated by GH. To determine whether GH-responsive IGF-I gene expression could be demonstrated in these cells, hepatocytes were treated without or with 50 ng/ml GH for 3--48 h. IGF-I mRNA levels increased within 3 h, and a maximal 2.2-fold increase was observed after 24 h of GH treatment. To determine whether ERK activation contributes to GH-induced IGF-I gene expression, hepatocytes were treated for 12 h without or with 50 ng/ml GH and 50 microM PD98059, an inhibitor of MAPK kinase-1 and -2. Treatment with PD98059 did not have a significant effect on GH-induced IGF-I gene expression. Similar studies were performed using 50 microM LY 294002, an inhibitor of PI3K. These studies demonstrated that treatment with LY 294002 completely abrogated GH-induced IGF-I gene expression. In contrast, PI3K-specific doses of another inhibitor of PI3K, wortmannin, failed to inhibit the GH-induced increase in IGF-I mRNA levels. In summary, rat hepatocytes in primary culture provide a good model system to study GH-induced IGF-I gene expression, and the results of these studies suggest that a signaling pathway inhibited by LY 294002, possibly a PI3K-dependent pathway, is important for GH-stimulated IGF-I gene expression in hepatocytes.

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