2. Vías de señalización
  3. PI3K/Akt/mTOR
  4. PI3K
  5. PI3Kα Isoform

PI3Kα

PI3Kα (p110α), encoded by PIK3CA, is a class IA phosphoinositide 3-kinase catalytic subunit that forms a heterodimer with p85 regulatory proteins and catalyzes the phosphorylation of phosphatidylinositol-(4,5)-bisphosphate to generate phosphatidylinositol-(3,4,5)-trisphosphate, thereby regulating cell growth, proliferation, survival, migration, and metabolic signaling[1][2]. Mechanistically, PI3Kα is a central component of the PI3K-AKT-mTOR signaling axis and functions downstream of receptor tyrosine kinases and RAS proteins to amplify intracellular growth and survival pathways[3][4]. Dysregulation of this pathway is among the most common molecular events in human cancer, and activating mutations in PIK3CA promote tumor initiation, progression, and therapeutic resistance through sustained PI3K signaling[3][5]. In disease models, disruption of the RAS-PI3Kα interaction suppresses tumor growth and angiogenesis, highlighting the importance of PI3Kα-dependent signaling in oncogenic processes[4]. Compared with related class I PI3K isoforms, p110α and p110β are broadly expressed across tissues, whereas p110δ is predominantly expressed in leukocytes, indicating distinct physiological functions and therapeutic opportunities among isoforms[6][7]. Furthermore, PTEN-deficient tumors frequently depend on p110β activity, emphasizing a biologically important distinction between PI3Kα- and PI3Kβ-driven signaling networks[8]. For experimental and translational applications, isoform-selective PI3Kα inhibitors, including alpelisib, have been developed to target PIK3CA-driven malignancies, making PI3Kα a major focus of precision oncology research[5].

PI3Kα Produits associés (225):

Cat. No. Nom du produit Effet Pureté
  • HY-143403
    PI3K-IN-31
    		Inhibitor 99.33%
    PI3K-IN-31 (Compound 6b) is a potent PI3K inhibitor with IC50s of 3.7 nM, 74 nM, 14.6 nM, and 9.9 nM for PI3Kα, PI3Kβ, PI3Kγ, and PI3Kδ, respectively. PI3K-IN-31 has anticancer effects.
  • HY-13514
    TG 100713
    		Inhibitor 99.21%
    TG 100713 is an inhibitor of PI3K, with IC50s of 24, 50, 165, and 215 nM for PI3Kδ, γ, α and β isoforms respectively.
  • HY-174461
    PROTAC PI3Kα degrader-1
    		Degrader 99.21%
    PROTAC PI3Kα degrader-1 is a PI3Kα PROTAC degrader (DC50 = 0.08 μM), demonstrating good selectivity for PI3Kα degradation over PI3Kβ, PI3Kγ, and PI3Kδ. PROTAC PI3Kα degrader-1 effectively degrades PI3Kα in a time- and concentration-dependent, over PI3Kβ, PI3Ky and PI3Kδ, and potently inhibited the phosphorylation of AKT at the Ser473site. PROTAC PI3Kα degrader-1 shows significant in vivo anticancer efficacy in HGC-27 and DOHH2 xenograft models. (Pink: PI3Kα ligand : (HY-174798), Blue: E3 ligase CRBN Ligand (HY-10984), Black: Linker, E3 ligase ligand-linker conjugate (HY-W940885)).
  • HY-10812
    GNE-490
    		Inhibitor
    GNE-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.
  • HY-12279C
    Umbralisib hydrochloride
    		Inhibitor 99.04%
    Umbralisib (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.
  • HY-11105
    Pilaralisib analogue
    		Inhibitor 99.74%
    Pilaralisib analogue (XL147 analogue) is a representative and selective PI3Kα inhibitor extracted from patent WO2012006552A1, Compound 147 in Table 1.
  • HY-111510
    IPI-3063
    		Inhibitor 99.59%
    IPI-3063 is a potent and selective PI3K p110δ inhibitor with an IC50 of 2.5 ± 1.2 nM.
  • HY-132231
    FD223
    		Inhibitor 98.05%
    FD223 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.
  • HY-147419
    Vulolisib
    		Inhibitor 99.61%
    Vulolisib is a potent and orally active phosphatidylinositol 3-kinase (PI3K) inhibitor, with IC50 values of 0.2 nM, 168 nM, 90 nM and 49 nM for PI3Kα, PI3Kβ, PI3Kγ and PI3Kδ, respectively. Antiproliferative and antineoplastic activity.
  • HY-112608
    CHMFL-PI3KD-317
    		Inhibitor 98.04%
    CHMFL-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.
  • HY-15271
    WYE-687
    		Inhibitor 98.05%
    WYE-687 is an ATP-competitive mTOR inhibitor with an IC50 of 7 nM. WYE-687 concurrently inhibits activation of mTORC1 and mTORC2. WYE-687 also inhibits PI3Kα and PI3Kγ with IC50s of 81 nM and 3.11 μM, respectively.
  • HY-12340
    ETP-46321
    		Inhibitor 99.34%
    ETP-46321 is a potent and orally bioavailable PI3Kα and PI3Kδ inhibitor with Kiapps of 2.3 and 14.2 nM, respectively.
  • HY-131345
    PI3Kα-IN-4
    		Inhibitor 99.76%
    PI3Kα-IN-4 is a potent, selective and orally active inhibitor of PI3Kα, with an IC50 of 1.8 nM. PI3Kα-IN-4 has antitumor activity.
  • HY-131345A
    (S)-PI3Kα-IN-4
    		Inhibitor 99.77%
    (S)-PI3Kα-IN-4 is a potent inhibitor of PI3Kα, with an IC50 of 2.3 nM. (S)-PI3Kα-IN-4 shows 38.3-, 4.25-, and 4.93-fold selectivity for PI3Kα over PI3Kβ, PI3Kδ, and PI3Kγ, respectively. (S)-PI3Kα-IN-4 can be used for the research of cancer.
  • HY-147284
    PI3K-IN-37
    		Inhibitor 99.0%
    PI3K-IN-37 (Example 84.1) is a PI3K α/β/δ inhibitor with IC50s of 6, 8, 4 nM, respectively. PI3K-IN-37 can also inhibit mTOR (IC50=4 nM).
  • HY-10620
    PI3K-IN-22
    		Inhibitor 99.50%
    PI3K-IN-22 is a PI3Kα/mTOR dual kinase inhibitor. PI3K-IN-22 has IC50s of 0.9, 0.6 nM for PI3Kα and mTOR, respectively. PI3K-IN-22 can be used for the research of cancer.
  • HY-110109
    ETP-45658
    		Inhibitor 98.97%
    ETP-45658 is a potent PI3K inhibitor, with IC50s of 22.0 nM, 39.8 nM, 129.0 nM and 717.3 nM for PI3Kα, PI3Kδ, PI3Kβ and PI3Kγ, respectively. ETP-45658 also can inhibit DNA-PK (IC50=70.6 nM) and mTOR (IC50=152.0 nM). ETP-45658 can be used for the research of cancer.
  • HY-11080A
    PKI-179 hydrochloride
    		Inhibitor 99.66%
    PKI-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.
  • HY-100603A
    (S)-GSK-F1
    		Inhibitor 98.01%
    (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.
  • HY-15269
    PP30
    		98.01%
    PP30 is a potent, selective, ATP-competitive mTOR inhibitor with an IC50 of 80 nM. PP30 blocks insulin-stimulated phosphorylation of Akt at residues S473 and T308, preventing the full activation of Akt. PP30 is applicable for cancer research.