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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Alpelisib (Standard)
0 ImagesSynonyms: BYL-719 (Standard)Alpelisib (BYL-719) (Standard) is the analytical standard of Alpelisib (HY-15244). This product is intended for research and analytical applications. Alpelisib (BYL-719) 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 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 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 can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome.
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GNE-490
0 ImagesCat. No.: HY-10812CAS No.: 1033739-92-2GNE-490, a (thienopyrimidin-2-yl)aminopyrimidine, is a potent pan-PI3K inhibitor with IC50s of 3.5 nM, 25 nM, 5.2 nM, 15 nM for PI3Kα, PI3Kβ, PI3Kδ and PI3Kγ, respectively. GNE-490 has >200 fold selectivity for mTOR (IC50=750 nM). GNE-490 shows potent suppression efficacy profile against MCF7.1 breast cancer xenograft model.
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Umbralisib hydrochloride
0 ImagesSynonyms: TGR-1202 hydrochloride; RP5264 hydrochlorideUmbralisib (TGR-1202) hydrochloride is an orally active, potent and selective dual PI3Kδ and casein kinase-1-ε (CK1ε) inhibitor, with EC50 of 22.2 nM and 6.0 μM, respectively. Umbralisib hydrochloride exhibits unique immunomodulatory effects on chronic lymphocytic leukemia (CLL) T cells. Umbralisib hydrochloride can be used for haematological malignancies reseach.
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FD223
0 ImagesFD223 is a potent and selective phosphoinositide 3-kinase delta (PI3Kδ) inhibitor. FD223 displays high potency (IC50=1 nM) and good selectivity over other isoforms (IC50s of 51 nM, 29 nM and 37 nM, respectively for α, β and γ). FD223 exhibits efficient inhibition of the proliferation of acute myeloid leukemia (AML) cell lines by suppressing p-AKT Ser473 thus causing G1 phase arrest during the cell cycle. FD223 has potential for the research of leukemia such as AML.
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CHMFL-PI3KD-317
0 ImagesCHMFL-PI3KD-317 is a highly potent, selective and orally active PI3Kδ inhibitor, with an IC50 of 6 nM, and exhibits over 10-1500 fold selectivity over other class I, II and III PIKK family isoforms, such as PI3Kα (IC50, 62.6 nM), PI3Kβ (IC50, 284 nM), PI3Kγ (IC50, 202.7 nM), PIK3C2A (IC50, >10000 nM), PIK3C2B (IC50, 882.3 nM), VPS34 (IC50, 1801.7 nM), PI4KIIIA (IC50, 574.1 nM) and PI4KIIIB (IC50, 300.2 nM). CHMFL-PI3KD-317 inhibits PI3Kδ-mediated Akt T308 phosphorylation in Raji cells, with an EC50 of 4.3 nM. CHMFL-PI3KD-317 has antiproliferative effects on cancer cells.
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(S)-GSK-F1
0 Images(S)-GSK-F1 (Compound 28) is an inhibitor for type III phosphatidylinositol 4-kinase α (PI4KIIIα). (S)-GSK-F1 inhibits PI4Kα, PI4Kβ, PI4Kγ, PI3Kα, PI3Kβ and PI3Kδ with pIC50 of 8.3, 6.0, 5.6, 5.6, 5.1 and 5.6, respectively. (S)-GSK-F1 exhibits anti-hepatitis C virus (HCV) activity through inhibition of HCV replication. (S)-GSK-F1 exhibits moderate pharmacokinetic characters in rat model.
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MIPS-9922
0 ImagesMIPS-9922 is a potent and selective PI3Kβ inhibitor with an IC50 of 63 nM. MIPS-9922 inhibits PI3Kβ with >30-fold higher potency than PI3Kδ. MIPS-9922 blocks PI3K mediated activation of platelet glycoprotein αIIbβ3 activation and platelet adhesion in vitro. MIPS-9922 shows anti-platelet and anti-thrombotic activities.
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PARP/PI3K-IN-1
0 ImagesPARP/PI3K-IN-1 (compound 15) is a potent PARP/PI3K inhibitor with pIC50 values of 8.22, 8.44, 8.25, 6.54, 8.13, 6.08 for PARP-1, PARP-2, PI3Kα, PI3Kβ, PI3Kδ, and PI3Kγ, respectively. PARP/PI3K-IN-1 is a highly effective anticancer compound targeted against a wide range of oncologic diseases.
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PKI-179 hydrochloride
0 ImagesPKI-179 hydrochloride 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 hydrochloride also exhibits activity over E545K and H1047R, with IC50s of 14 nM and 11 nM, respectively. PKI-179 hydrochloride shows anti-tumor activity in vivo.
