PI3Kβ
PI3Kβ is a class I PI3K catalytic isoform that produces PIP3, linking receptor inputs to signaling networks that regulate cell growth, survival, and movement[1]. Mechanistically, PI3Kβ uniquely supports synergistic PIP3 formation when GPCR and RTK pathways are coactivated in myeloid cells, whereas p110α, p110β, and p110δ show partial redundancy downstream of M-CSF alone and p110γ acts nonredundantly downstream of C5a alone[1]. In PTEN-deficient breast tumour models, PI3Kβ inactivation reduced STAT3 signaling, increased immune-stimulatory molecules, and promoted anti-tumour immune responses[2]. Compared with related PI3K isoforms, this evidence positions PI3Kβ as a context-specific integrator of coincident receptor signaling and a disease-relevant driver in PTEN-null tumours[1][2]. For experimental applications, the PI3Kβ-selective inhibitor KIN-193 blocked AKT signaling and tumour growth dependent on p110β activation or PTEN loss, while pharmacological PI3Kβ inhibition also synergized with immunotherapy in PTEN-null breast tumour models[3][2].
References:
- [1]. Houslay DM, et al. Coincident signals from GPCRs and receptor tyrosine kinases are uniquely transduced by PI3Kβ in myeloid cells. Sci Signal. 2016 Aug 16;9(441):ra82. [Content Brief]
- [2]. Bergholz JS, et al. PI3Kβ controls immune evasion in PTEN-deficient breast tumours. Nature. 2023 May;617(7959):139-146. [Content Brief]
- [3]. 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]
All Product Categories
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PI3Kβ Related Products (162)
Related Products (162)
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PKI-179
0 ImagesPKI-179 is a potent and orally active dual PI3K/mTOR inhibitor, with IC50s of 8 nM, 24 nM, 74 nM, 77 nM, and 0.42 nM for PI3K-α, PI3K-β, PI3K-γ, PI3K-δ and mTOR, respectively. PKI-179 also exhibits activity over E545K and H1047R, with IC50s of 14 nM and 11 nM, respectively. PKI-179 shows anti-tumor activity in vivo.
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Izorlisib
0 ImagesSynonyms: CH5132799Izorlisib (CH5132799) is an orally active, selective Class I PI3K inhibitor with an IC50 value of 14 nM against PI3Kα. Izorlisib specifically inhibits Class I PI3K (particularly PI3Kα and its mutants) and blocks the PI3K/Akt/mTOR pathway; this leads to cell cycle arrest at the G1 phase and apoptosis without triggering feedback activation of Akt by competitively binding to the ATP-binding site of PI3K. Izorlisib can be used in research on cancers harboring PIK3CA mutations or PTEN loss (such as breast, ovarian, prostate, and endometrial cancers).
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PF-06843195
0 ImagesPF-06843195 is a highly selective PI3Kα inhibitor with an IC50 of 18 nM in Rat1 fibroblasts. The Kis of PF-06843195 for PI3Kα and PI3Kδ in biochemical kinase assay are less than 0.018 nM and 0.28 nM, respectively. PF-06843195 has great suppression of the PI3K/mTOR signaling pathway and durable antitumor efficacy.
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Alpelisib hydrochloride
0 ImagesSynonyms: BYL-719 hydrochlorideAlpelisib (BYL-719) hydrochloride is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib hydrochloride also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib hydrochloride not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib hydrochloride can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome.
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PI3K/mTOR Inhibitor-4
0 ImagesCat. No.: HY-128333CAS No.: 2361215-32-7
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PI3Kα-IN-9
0 ImagesCat. No.: HY-150618CAS No.: 2715287-67-3
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SRX3177
0 ImagesSRX3177 is a triple inhibitor of CDK4/6, PI3K, and BRD4, with IC50s of <2.5 nM (CDK4), 3.3 nM (CDK6), 33 nM (BRD4 BD1), 89 nM (BRD4 BD2), 79 nM (PI3Kα), 83 nM (PI3Kδ), 3.18 μM (PI3Kγ) , respectively. SRX3177 blocks the interaction between the SARS-CoV-2 E protein and the BRD2/4 BD1 domain, restores E protein-attenuated NF-κB activity. SRX3177 exerts broad cytotoxic activity against cancer cells. SRX3177 can be used for the study of anti-SARS-CoV-2 and cancer.
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KTC1101
0 ImagesKTC1101 is an orally active pan-PI3K inhibitor. KTC1101 can inhibit the PI3K signaling pathway, reduce downstream AKT and mTOR phosphorylation, and reduces the expression of Ki67. The anti-tumor effect of KTC1101 has a dual mechanism of action: directly inhibiting tumor cell growth and dynamically enhancing immune response.
