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novel pi3k inhibitor

Taken together, our findings establish B591, a novel PI3K inhibitor, as a strong candidate for clinical evaluation as a CSCs targeting agent.

B591, a novel specific pan-PI3K inhibitor, preferentially targets cancer stem cells

novel pi3k inhibitor

The search for novel PI3K inhibitors has been at the forefront of academic and industrial medicinal chemistry with over 600 medicinal chemistry-based publications and patents appearing to date, leading to 38 clinical candidates and the launch of two drugs, idelalisib in 2014 and copanlisib in 2017.

Class 1 PI3K Clinical Candidates and Recent Inhibitor Design Strategies: A Medicinal Chemistry Perspective.

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10.1016/j.cbi.2019.01.026

In conclusion, our results show a novel PI3K-independent effect of buparlisib that may improve therapeutic efficacy and safety of daunorubicin by preventing its metabolism by AKR1C3.

Buparlisib is a novel inhibitor of daunorubicin reduction mediated by aldo-keto reductase 1C3.

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10.1038/s41392-019-0085-2

CYH33 is a novel PI3Kα-selective inhibitor in phase I clinical trials (NCT03544905) and exhibits potent activity against breast cancer in preclinical settings.

Unbiased screening reveals that blocking exportin 1 overcomes resistance to PI3Kα inhibition in breast cancer

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10.1158/1535-7163.TARG-19-A116

CYH33 is a novel PI3Kα-selective inhibitor and displays promising efficacy against ESCC in preclinical settings, which is currently in phase I clinical trial for the treatment of ESCC.

Abstract A116: HRASG12S mutant mediates resistance to a PI3Kα inhibitor CYH33 in esophageal squamous cell carcinomas

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10.1158/1538-7445.AM2019-529

As PI3Kα controls a key oncogenic signaling pathway, we evaluated whether RT or novel PI3Kαδ inhibitor or both could enhance the efficacy of antitumor effect of a PD-1 blockade in immune competent syngenic triple negative breast cancer (TNBC) model.

Abstract 529: A PI3Kαδ inhibitor combined with irradiation enhance the effect of PD-1 blockade in syngenic triple negative breast cancer model

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10.2174/1573406415666190222125333

CONCLUSIONS Crystallography-based pharmacophores were successfully combined with QSAR analysis for the identification of novel PI3Kδ inhibitors.

Discovery of new Phosphoinositide 3-kinase delta (PI3Kδ) inhibitors via virtual screening using crystallography-derived pharmacophore modelling and QSAR analysis.

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10.1021/acs.jmedchem.9b00390

Herein, we have discovered a series of novel PI3K and HDAC dual inhibitors in which the hydroxamic acid moiety as the zinc binding functional group was introduced to a quinazoline-based PI3K pharmacophore through an appropriate linker.

Design, Synthesis, and Biological Evaluation of 4-Methyl Quinazoline Derivatives as Anticancer Agents Simultaneously Targeting Phosphoinositide 3-Kinases and Histone Deacetylases.

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10.4062/biomolther.2019.153

PBT-6, a novel PI3KC2γ inhibitor, decreased the cell growth of TNF-mediated synovial fibroblasts and LPS-mediated macrophages.

PBT-6, a Novel PI3KC2γ Inhibitor in Rheumatoid Arthritis

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10.1016/j.intimp.2019.105756

AS2541019 is a novel PI3Kδ selective inhibitor that prevents antibody production by inhibiting B cell immunity.

The PI3Kδ selective inhibitor AS2541019 suppresses donor-specific antibody production in rat cardiac and non-human primate renal allotransplant models.

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10.1021/acsmedchemlett.8b00530

We have developed a synthesis of a novel PI3Kγ inhibitor containing a 1,2-dihydro-3H-pyrrolo[3,4-c]pyridin-3-one scaffold.

Synthesis of a 6-Aza-Isoindolinone-Based Inhibitor of Phosphoinositide 3-Kinase γ via Ruthenium-Catalyzed [2 + 2 + 2] Cyclotrimerization.

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10.1016/j.bioorg.2019.103525

Herein, we synthesized a new series of substituted 2-(thiophen-2-yl)-1,3,5-triazine derivatives as novel PI3Kα/mTOR dual inhibitors for cancer therapy.

Design, synthesis and biological evaluation of substituted 2-(thiophen-2-yl)-1,3,5-triazine derivatives as potential dual PI3Kα/mTOR inhibitors.

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10.1080/17425255.2019.1663169

A summary of mechanisms underlying the adverse effects is not only significant for the development of novel PI3K/AKT/mTOR inhibitors but also beneficial for the optimal use of existing drugs.

Molecular basis for class side effects associated with PI3K/AKT/mTOR pathway inhibitors

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10.7150/thno.35561

Using specific protein interactome strategy by BirA proximity-dependent biotin identification, we demonstrated that FKBP4 is a novel PI3K-Akt-mTOR proximal interacting protein.

FKBP4 connects mTORC2 and PI3K to activate the PDK1/Akt-dependent cell proliferation signaling in breast cancer

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10.3390/cancers11050627

In our previous study, we rationally designed and synthesized DFX117(6-(5-(2,4-difluorophenylsulfonamido)-6-methoxypyridin-3-yl)-N-(2-morpholinoethyl) imidazo[1,2-a]pyridine-3-carboxamide) as a novel PI3Kα selective inhibitor.

Antitumor Activity of DFX117 by Dual Inhibition of c-Met and PI3Kα in Non-Small Cell Lung Cancer

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Novel Pi3k - In conclusion, our results show a novel PI3K-independent effect of buparlisib that may improve therapeutic efficacy and safety of daunorubicin by preventing its metabolism by AKR1C3. [1] CYH33 is a novel PI3Kα-selective inhibitor in phase I clinical trials (NCT03544905) and exhibits potent activity against breast cancer in preclinical settings. [2] CYH33 is a novel PI3Kα-selective inhibitor and displays promising efficacy against ESCC in preclinical settings, which is currently in phase I clinical trial for the treatment of ESCC. [3] As PI3Kα controls a key oncogenic signaling pathway, we evaluated whether RT or novel PI3Kαδ inhibitor or both could enhance the efficacy of antitumor effect of a PD-1 blockade in immune competent syngenic triple negative breast cancer (TNBC) model. [4] CONCLUSIONS Crystallography-based pharmacophores were successfully combined with QSAR analysis for the identification of novel PI3Kδ inhibitors. [5] Herein, we have discovered a series of novel PI3K and HDAC dual inhibitors in which the hydroxamic acid moiety as the zinc binding functional group was introduced to a quinazoline-based PI3K pharmacophore through an appropriate linker. [6] PBT-6, a novel PI3KC2γ inhibitor, decreased the cell growth of TNF-mediated synovial fibroblasts and LPS-mediated macrophages. [7] AS2541019 is a novel PI3Kδ selective inhibitor that prevents antibody production by inhibiting B cell immunity. [8] We have developed a synthesis of a novel PI3Kγ inhibitor containing a 1,2-dihydro-3H-pyrrolo[3,4-c]pyridin-3-one scaffold. [9] Herein, we synthesized a new series of substituted 2-(thiophen-2-yl)-1,3,5-triazine derivatives as novel PI3Kα/mTOR dual inhibitors for cancer therapy. [10] A summary of mechanisms underlying the adverse effects is not only significant for the development of novel PI3K/AKT/mTOR inhibitors but also beneficial for the optimal use of existing drugs. [11] Using specific protein interactome strategy by BirA proximity-dependent biotin identification, we demonstrated that FKBP4 is a novel PI3K-Akt-mTOR proximal interacting protein. [12] In our previous study, we rationally designed and synthesized DFX117(6-(5-(2,4-difluorophenylsulfonamido)-6-methoxypyridin-3-yl)-N-(2-morpholinoethyl) imidazo[1,2-a]pyridine-3-carboxamide) as a novel PI3Kα selective inhibitor. [13]

novel pi3k inhibitor

Taken together, our findings establish B591, a novel PI3K inhibitor, as a strong candidate for clinical evaluation as a CSCs targeting agent. [1] The search for novel PI3K inhibitors has been at the forefront of academic and industrial medicinal chemistry with over 600 medicinal chemistry-based publications and patents appearing to date, leading to 38 clinical candidates and the launch of two drugs, idelalisib in 2014 and copanlisib in 2017. [2] Furthermore, novel PI3K inhibitors, such as idelalisib and copanlisib, have shown impressive clinical activity in several indolent lymphomas including marginal zone lymphoma (MZL). [3] Recently, lipomas associated with PIK3CA-related overgrowth syndrome were successfully treated with the novel PI3K inhibitor alpelisib. [4] In this context, after promising preclinical data on the novel PI3K inhibitor BYL719, the NCT01735968 trial in GIST patients who had previously failed treatment with imatinib and sunitinib started. [5]