NVP-BQR695 is a novel PI3K inhibitor.

OTSSP167 is a highly potent MELK inhibitor (IC50 = 0.41 nM) and inhibited the phosphorylation of PSMA1 (proteasome subunit alpha type 1) and DBNL (drebrin-like).

PF-4989216 is a potent and selective PI3K inhibitor with IC50 of 2 nM, 142 nM, 65 nM, 1 nM, and 110 nM for p110α, p110β, p110γ, p110δ, and VPS34, respectively.

PIK-293 is a PI3K inhibitor, mostly for PI3Kδ with IC50 of 0.24 μM, 500-, 100- and 50-fold less potent to PI3Kα/β/γ, respectively.

PQR530 is a selective, orally bioavailable, potent dual PI3K/mTORC1/2 inhibitor.

PP30, a TORKinib, is a potent, selective, and ATP-competitive inhibitor of mTOR with an IC50 of 80 nM.

MS143 is a potent AKT degrader (DC50=46 nM and GI50=0.8 µM in PC3 cells). MS143 induces rapid and robust AKT degradation in a concentration- and time-dependent manner via hijacking the ubiquitin-proteasome system. MS143 can suppress cancer cell growth.

CC214-2 is a potent and dual inhibitor of mTORC1/mTORC2. Mycobacterium tuberculosis modulates mammalian target of rapamycin (mTOR) signaling to impede autophagy. CC214-2 has the potential to shorten the duration of TB.

Seco-rapamycin(Secorapamycin A) is the first in vivo open-ring metabolite of rapamycin that does not affect mTOR..

SF2523 is a highly selective and potent inhibitor of PI3K and BRD4with IC50 values of 16 and 241 nM for PI3Kα and BD1, respectively.

TAK-117(INK1117,MLN1117) is an orally bioavailable inhibitor of the class I phosphoinositide 3-kinase (PI3K) alpha isoform with potential antineoplastic activity.

Deforolimus(AP23573; MK-8669; Ridaforolimus) is a selective mTOR inhibitor with IC50 of 0.2 nM; while not classified as a prodrug, mTOR inhibition and FKBP12 binding is similar to rapamycin. IC50 value: 0.2 nM [1] Target: mTOR in vitro: Treatment of HT

Pipinib is a small molecule Hedgehog signaling inhibitior by selective inhibition of phosphatidylinositol 4-kinase IIIβ (PI4KB, IC50=2.2 uM), inhibits Purmorphamine-induced osteogenesis with IC50 of 0.6 uM.Pipinib inhibited GLI reporter gene activity in Sonic hedgehog (Shh)-LIGHT2 cells (IC50=1.7 uM) and expression of Hh target genes Ptch1 and Gli1 (IC50=3.1 uM and 4.1 uM, respectively).Pipinib does not modulate Hh signaling via SMO.Pipinib is an ATP-competitive inhibitor of PI4KB activity, does not inhibit isoenzymes PI4KA, PI4K2A or PI4K2B up to 50 uM.Pipinib suppresses GLI-mediated transcription and Hh target gene expression by impairing SMO translocation to the cilium.

HTH-02-006 is a potent, selective reversible inhibitor of NUAK1/2 with binding IC50 of 8/126 nM, respectively.HTH-02-006 reduces MYPT1(S445) phosphorylation in HuCCT-1 cells, suggesting NUAK1/2 inhibition.HTH-02-006 ameliorates YAP(S127A)-induced hepatomegaly, and reduces MYPT1(S445) phosphorylation.HTH-02-006 delays the outgrowth of YAP-induced HuCCT-1 xenograft tumors in nude mice.HTH-02-006 downregulated E2F, EMT, and MYC hallmark gene sets after NUAK2 inhibition in PC cells.HTH-02-006 slowed tumor growth and proliferation rates in a syngeneic allograft model and in radical prostatectomy patient derived explants.HTH-02-006 treatment led to inactivation of YAP and the downregulation of NUAK2 and MYC protein levels.

FAPL-PI3Ki1 is a specific FAP-targeted PI3K inhibitor that selectively targets FAP-expressing human IPF lung fibroblasts and potently inhibits collagen synthesis.FAPL-PI3Ki1 significantly inhibited phosphorylation of Akt in IPF fibroblasts with IC50 of 200 nM, also inhibited phosphorylation of 4E-BP1.FAPL-PI3Ki1 induced suppression of TGFb1-stimulated collagen production and phosphorylation of Akt in IPF fibroblasts requires participation of FAP.FAPL-PI3Ki1 suppressed production of hydroxyproline (major building block of collagen), reduced collagen deposition, and increased mouse survival in a mouse model of IPF inhibited PI3K activation in fibrotic lungs.

CPL302-253 is a potent, selective inhibitor of PI3Kδ with IC50 of 12.2 nM and Kd of 0.83 nM, >350-fold selectivity over PI3K isoforms α, β, and γ (IC50>4,500 nM); CPL302-253 displays no off-target interaction in KinomeScan assays. CLP302-253 blocks activation of primary lymphoid cells in vitro, blocks IL-33 cytokine production in epithelial and T cell co-cultures. CLP302-253 bocks eosinophil infiltration to the lungs and IL-33 expression in HDM induced asthma mouse model.

AZ7 (PI4KA inhibitor 7) is a potent, selective PI4KA inhibitor with pIC50 of 8.2, >100-fold selectivity over PI4Kβ, PI3Kα and PIP5Kγ.AZ7 inhibited the accumulation of IP1 (pIC50 6.3) caused a qualitative reduction in cellular PIP, PIP2 and PIP3 levels.PI4KA inhibitor 7 inhibited cell growth with pGI50 values of >5.0 in 91 of the cell lines in a panel of 183 cancer cell lines.

AZ3 (PI4KB inhibitor 3) is a seletive PI4KB inhibitor with pIC50 of 7.8, shows good lipid kinase selectivity (pIC50 5.1, 4.7 and 4.0 for PI4Kα, PI3Kα and PIP5Kγ respectively).

A-674563 is a potent, selective and orally available AKT inhibitor with Ki of 11 nM (Akt1); increases the efficacy of paclitaxel in a PC-3 xenograft model; enhances the transcription of several chondrocyte marker genes, including Col2a1, Acan and Col11a2, in mouse primary chondrocytes by inhibiting Sox9 degradation through the ubiquitin-proteasome pathway; also suppresses FLT3-ITD positive AML both in vitro and in vivo.

Viridin is a secondary metabolite and naturally occurring furanosteroid. Viridin is potent inhibitor of the lipid kinase PI3K.

PI3Kδ/γ-IN-1 is a potent, selective PI3K-δ/γ inhibitor for treatment of hematological malignancies.

PI3K-IN-26 is a potent PI3K inhibitor with an IC50 of 36 nM for SU-DHL-6 cells (WO2016066142A1, compound 1).

10Z-Hymenialdisine ((Z)-Hymenialdisine) is a natural bioactive pyrrole alkaloid. 10Z-Hymenialdisine is a pan kinase inhibitor, and has anticancer activities.

AKT-IN-10 is a potent inhibitor of AKT. Protein kinase B (PKB, also known as AKT) is central to PI3K/AKT/mTOR signaling in cells, and its function is important for cell growth, survival, differentiation and metabolism. AKT-IN-10 has the potential for the research of breast and prostate cancer (extracted from patent WO2021185238A1, compound 4).

AKT-IN-9 is a potent inhibitor of AKT. Protein kinase B (PKB, also known as AKT) is central to PI3K/AKT/mTOR signaling in cells, and its function is important for cell growth, survival, differentiation and metabolism. AKT-IN-9 has the potential for the research of breast and prostate cancer (extracted from patent WO2021185238A1, compound 1).

PI3K/AKT-IN-1 is an effective PI3K/AKT dual inhibitor (IC50 of 6.99, 4.01 and 3.36 μM for PI3Kγ, PI3Kδ and AKT, respectively). PI3K/AKT-IN-1 has anticancer activity and acts by inhibiting PI3K/AKT axis and inducing caspase 3 dependent apoptosis.

PI3K-IN-29 is a potent PI3K inhibitor. PI3K-IN-29 displays good inhibition potencies against U87MG, HeLa and HL60 cells with IC50 values of 0.264, 2.04 and 1.14 µM, respectively. PI3K-IN-29 inhibits PI3K/Akt pathway by inhibiting phosphorylation of Akt that is catalyzed by PI3K.

PI3K-IN-27 is a potent inhibitor of PI3K. PI3K belongs to a large family of lipid signaling kinase that plays key role in cellular process including cell growth, differentiation, migration and apoptosis. PI3K-IN-27 has the potential for the research of hyper-proliferative diseases like cancer and inflammation, or immune and autoimmune diseases (extracted from patent WO2021233227A1, compound 1).

PI3K-IN-30 (compound 6d) is a potent PI3K inhibitor with IC50s of 5.1, 136, 30.7 and 8.9 nM for PI3Kα, PI3Kβ, PI3Kγ and PI3Kδ, respectively.

PI3Ka-IN-5 (compound 6 ab) is a potent PI3Kα/mTOR inhibitor, with an IC50 of 0.7 nM and 3.3 nM, respectively. PI3Ka-IN-5 can be used for the research of colorectal cancer.