Last update 01 Nov 2024

IP6K3

Last update 01 Nov 2024

Basic Info

Synonyms

IHPK3, inositol hexakisphosphate kinase 3, Inositol hexaphosphate kinase 3

+ [3]

Introduction

Converts inositol hexakisphosphate (InsP6) to diphosphoinositol pentakisphosphate (InsP7/PP-InsP5). Converts 1,3,4,5,6-pentakisphosphate (InsP5) to PP-InsP4.

Drugs associated with IP6K3

SCO-006

Target

IP6K1 x IP6K2 x IP6K3

Mechanism

IP6K1 inhibitors [+2]

Active Org.

SCOHIA PHARMA, Inc.Startup

Originator Org.

Takeda Pharmaceutical Co., Ltd.

Active Indication

Ovarian clear cell carcinoma

Inactive Indication

Hyperphosphatemia

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with IP6K3

100 Translational Medicine associated with IP6K3

0 Patents (Medical) associated with IP6K3

195

Literatures (Medical) associated with IP6K3

01 Jul 2024·EFSA Journal

Safety evaluation of the food enzyme 3‐phytase from the non‐genetically modified Aspergillus niger strain PHY93‐08

Article

Author: Kovalkovicova, Natalia ; Chesson, Andrew ; Roos, Yrjo ; Gott, David Michael ; EFSA Panel on Food Contact Materials, Enzymes and Processing Aids ; Vernis, Laurence ; Crebelli, Riccardo ; Cocconcelli, Pier Sandro ; Bolognesi, Claudia ; Mengelers, Marcel ; Barat Baviera, Jose Manuel ; Glandorf, Boet ; Lampi, Evgenia ; Lambre, Claude ; Steffensen, Inger-Lise ; Lunardi, Simone ; Zorn, Holger ; Liu, Yi ; Van Loveren, Henk ; Andryszkiewicz, Magdalena ; Grob, Konrad ; Tlustos, Christina ; Riviere, Gilles ; Mortensen, Alicja

Abstract The food enzyme 3‐phytase (myo‐inositol‐hexakisphosphate 3‐phosphohydrolase EC 3.1.3.8) is produced with the non‐genetically modified Aspergillus niger strain PHY93‐08 by Shin Nihon Chemical Co., Ltd. The food enzyme is free from viable cells of the production organism. It is intended to be used in nine food manufacturing processes. Since residual amounts of food enzyme–total organic solids (TOS) are removed in two of the food manufacturing processes, dietary exposure was calculated only for the remaining seven processes. It was estimated to be up to 0.763 mg TOS/kg body weight (bw) per day in European populations. Genotoxicity tests did not raise safety concerns. The systemic toxicity was assessed by means of a repeated dose 90‐day oral toxicity study in rats. The Panel identified a no observed adverse effect level of 2560 mg TOS/kg bw per day, the highest dose tested, which when compared with the estimated dietary exposure, resulted in a margin of exposure of at least 3355. A search for the similarity of the amino acid sequence of the food enzyme to known allergens was made and no matches were found. The Panel considered that the risk of allergic reactions upon dietary exposure cannot be excluded, but the likelihood is low. Based on the data provided, the Panel concluded that this food enzyme does not give rise to safety concerns under the intended conditions of use.

01 Jun 2024·Zhongguo shi yan xue ye xue za zhi

[Whole Exome Sequencing Reveals Gene Mutation Characteristics of Primary Central Nervous System Lymphoma].

Article

Author: Zhang, Li-Tian ; Han, Ye ; Li, Cui-Cui ; Wu, Chong-Yang ; Jin, Qi-Qi ; Jiang, Hao-Yun

OBJECTIVETo investigate gene mutation characteristics of primary central nervous system lymphoma (PCNSL) through whole exome sequencing (WES) to 18 patients with PCNSL.METHODSTumor tissues from 18 patients with diffuse large B-cell lymphoma who were diagnosed with PCNSL in Department of Hematology, Lanzhou University Second Hospital from September 2018 to December 2020 and had normal immune function, no history of HIV or immunosuppressant therapy were collected. High-throughput-based WES was performed on the tumor tissues, with an average sequencing depth of >100×. After data processing and bioinformatics analysis of sequencing results, the mutation maps and mutation characteristics of 18 PCNSL patients were obtained.RESULTSObvious somatic mutations were detected in all 18 patients. The median number of somatic mutations was 321. Missense mutations were most prominent (accounting for about 90%), and the mutation type was dominated by C>T (50.2%), reflecting the age-related mutation pattern. Among the top 15 frequently mutated genes, PSD3, DUSP5, MAGEB16, TELO2, FMO2, TRMT13, AOC1, PIGZ, SVEP1, IP6K3, and TIAM1 were the driver genes. The enrichment results of driver gene pathways showed that RTK-RAS, Wnt, NOTCH, Hippo and Cell-Cycle pathways were significantly enriched. The tumor mutation burden was between 3.558 48/Mb and 8.780 89/Mb, and the average was 4.953 32/Mb, which was significantly higher than other cancer research cohorts in the TCGA database.CONCLUSIONSPCNSL occurs somatic missense mutations frequently, mainly point mutations, and the mutation type is mainly C>T. The driver genes are mainly involved in RTK-RAS, Wnt, NOTCH and Hippo pathways, indicating that the above pathways may be related to the pathogenesis of PCNSL. PCNSL has a significantly high tumor mutation burden, which may explain the efficacy of PD-1 inhibitors in PCNSL.

01 Apr 2024·Journal of Lipid Research

Cholesterol trafficking to the ER leads to the activation of CaMKII/JNK/NLRP3 and promotes atherosclerosis

Article

Author: Tall, Alan R ; Westerterp, Marit ; Yalcinkaya, Mustafa ; Wang, Nan ; Xiao, Tong ; Liu, Wenli ; Abramowicz, Sandra ; Wang, Ranran

The deposition of cholesterol-rich lipoproteins in the arterial wall triggers macrophage inflammatory responses, which promote atherosclerosis. The NLRP3 inflammasome aggravates atherosclerosis; however, cellular mechanisms connecting macrophage cholesterol accumulation to inflammasome activation are poorly understood. We investigated the mechanisms of NLRP3 inflammasome activation in cholesterol-loaded macrophages and in atherosclerosis-prone Ldlr^-/- mice with defects in macrophage cholesterol efflux. We found that accumulation of cholesterol in macrophages treated with modified LDL or cholesterol crystals, or in macrophages defective in the cholesterol efflux promoting transporters ABCA1 and ABCG1, leads to activation of NLRP3 inflammasomes as a result of increased cholesterol trafficking from the plasma membrane to the ER, via Aster-B. In turn, the accumulation of cholesterol in the ER activates the inositol triphosphate-3 receptor, CaMKII/JNK, and induces NLRP3 deubiquitylation by BRCC3. An NLRP3 deubiquitylation inhibitor or deficiency of Abro1, an essential scaffolding protein in the BRCC3-containing cytosolic complex, suppressed inflammasome activation, neutrophil extracellular trap formation (NETosis), and atherosclerosis in vivo. These results identify a link between the trafficking of cholesterol to the ER, NLRP3 deubiquitylation, inflammasome activation, and atherosclerosis.

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IP6K3

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