Last update 01 Nov 2024

IMPA2

Last update 01 Nov 2024

Basic Info

Synonyms

IMP 2, IMP.18P, IMPA2

+ [6]

Introduction

Can use myo-inositol monophosphates, scylloinositol 1,4-diphosphate, glucose-1-phosphate, beta-glycerophosphate, and 2'-AMP as substrates. Has been implicated as the pharmacological target for lithium Li(+) action in brain.

Drugs associated with IMPA2

Lithium carbonate

Target

IMPA2

Mechanism

IMPA2 modulators

Active Org.

ANI Pharmaceuticals, Inc. [+3]

Originator Org.

Solvay SA

Active Indication

Bipolar I disorder [+2]

Inactive Indication

Schizoaffective disorder

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

First Approval Date06 Apr 1970

HG-1052

Target

IMPA2

Mechanism

IMPA2 modulators

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Nervous System Diseases

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with IMPA2

IRCT20240621062198N1 / SuspendedPhase 2IIT

Comparing the Effect of Sodium valproate with Lithium carbonate on Suicidal Ideation of Patients with Bipolar Disorder in Manic Phase with Mediation of Interoception

Start Date22 Oct 2024

Sponsor / Collaborator

Mashhad University of Medical Sciences

IRCT20130313012810N38 / CompletedIIT

Comparative bioequivalence study of the Lithium carbonate 300-mg Tablets manufactured by Vana Darou Gostar Pharmaceutical Company

Start Date19 Sep 2024

Sponsor / Collaborator-

NCT06184581 / RecruitingPhase 4IIT

Lithium Versus Lamotrigine in Bipolar Disorder, Type II - a Single Blinded Randomized Controlled Trial (the LiLa-Bipolar RCT)

The investigators want in a 6-month randomized controlled trial (RCT) to compare effects of lithium versus lamotrigine on mood stabilization and other critical patient outcomes in patients with BDII.

Start Date08 May 2024

Sponsor / Collaborator-

100 Clinical Results associated with IMPA2

100 Translational Medicine associated with IMPA2

0 Patents (Medical) associated with IMPA2

233

Literatures (Medical) associated with IMPA2

01 Aug 2024·CNS Neuroscience & Therapeutics

Long noncoding RNA H19 knockdown promotes angiogenesis via IMP2 after ischemic stroke

Article

Author: Yang, Zhenhong ; Wang, Rongliang ; Liu, Ping ; Li, Lingzhi ; Zheng, Yangmin ; Zhong, Liyuan ; Hu, Yue ; Fan, Junfen ; Yan, Feng ; Luo, Yumin

AbstractAimsThis study aimed to explore the effects of long noncoding RNA (lncRNA) H19 knockdown on angiogenesis and blood–brain barrier (BBB) integrity following cerebral ischemia/reperfusion (I/R) and elucidate their underlying regulatory mechanisms.MethodsA middle cerebral artery occlusion/reperfusion model was used to induce cerebral I/R injury. The cerebral infarct volume and neurological impairment were assessed using 2,3,5‐triphenyl‐tetrazolium chloride staining and neurobehavioral tests, respectively. Relevant proteins were evaluated using western blotting and immunofluorescence staining. Additionally, a bioinformatics website was used to predict the potential target genes of lncRNA H19. Finally, a rescue experiment was conducted to confirm the potential mechanism.ResultsSilencing of H19 significantly decreased the cerebral infarct volume, enhanced the recovery of neurological function, mitigated BBB damage, and stimulated endothelial cell proliferation following ischemic stroke. Insulin‐like growth factor 2 mRNA‐binding protein 2 (IMP2) is predicted to be a potential target gene for lncRNA H19. H19 knockdown increased IMP2 protein expression and IMP2 inhibition reversed the protective effects of H19 inhibition.ConclusionDownregulation of H19 enhances angiogenesis and mitigates BBB damage by regulating IMP2, thereby alleviating cerebral I/R injury.

01 Jun 2024·Journal of Affective Disorders

Pathogenesis or a response to lithium? A novel perspective for mitochondrial mass fluctuation of naïve T cells in patients with bipolar disorder

Article

Author: Li, Wanzhen ; Huang, Yiran ; Wang, Xiaofan ; Wang, Bingqi ; Chen, Zhenni ; Wang, Min

BACKGROUNDImmune imbalances are associated with the pathogenesis and pharmacological efficacy of bipolar disorder (BD). The underlying mechanisms remain largely obscure but may involve immunometabolic dysfunctions of T-lymphocytes.METHODSWe investigated if inflammatory cytokines and the immunometabolic function of T-lymphocytes, including frequencies of subsets, mitochondrial mass (MM), and low mitochondrial membrane potential (MMP^Low) differed between BD patients (n = 47) and healthy controls (HC, n = 43). During lithium treatment of hospitalized patients (n = 33), the association between weekly T-lymphocyte immune metabolism and clinical symptoms was analyzed, and preliminary explorations on possible mechanisms were conducted.RESULTSIn comparison to HC, BD patients predominantly showed a trend toward CD4⁺ naïve T (Tn) activation and exhibited mitochondrial metabolic disturbances such as decreased MM and increased MMP^Low. Lower CD4⁺ Tn-MM correlated with elevated IL-6, IL-8, and decreased IL-17 A in BD patients. With lithium treatment effective, MM of CD4⁺ T/Tn was negatively correlated with depression score HAMD. When lithium intolerance was present, MM of CD4⁺ T/Tn was positively correlated with depression score HAMD and mania score BRMS. Lithium does not mediate through the inositol depletion hypothesis, but the mRNA level of IMPA2 in peripheral blood is associated with mitochondrial function in CD8⁺ T cells.LIMITATIONSThe cross-sectional design and short-term follow-up meant that we could not directly examine the causality of BD and immune dysregulation.CONCLUSIONThe altered metabolism of CD4⁺ Tn was strongly associated with remodeling of the inflammatory landscape in BD patients and can also be used to reflect the short-term therapeutic effects of lithium.

01 Feb 2024·Cancer Letters

IMPA2 promotes basal-like breast cancer aggressiveness by a MYC-mediated positive feedback loop

Article

Author: Bai, Longchang ; Wu, Xuebiao ; Ma, Chenglong ; Li, Jun ; Deng, Xinyue ; Ma, Yihua ; Liao, Ruocen ; Dong, Chenfang ; Cao, Qianhua ; Lei, Xingyu ; Wang, Zhenzhen ; Dai, Zhijun ; Chen, Xingyu

Basal-like breast cancer (BLBC) is the most aggressive subtype with poor prognosis; however, the mechanisms underlying aggressiveness in BLBC remain poorly understood. In this study, we showed that in contrast to other subtypes, inositol monophosphatase 2 (IMPA2) was dramatically increased in BLBC. Mechanistically, IMPA2 expression was upregulated due to copy number amplification, hypomethylation of IMPA2 promoter and MYC-mediated transcriptional activation. IMPA2 promoted MI-PI cycle and IP3 production, and IP3 then elevated intracellular Ca²⁺ concentration, leading to efficient activation of NFAT1. In turn, NFAT1 up-regulated MYC expression, thereby fulfilling a positive feedback loop that enhanced aggressiveness of BLBC cells. Knockdown of IMPA2 expression caused the inhibition of tumorigenicity and metastasis of BLBC cells in vitro and in vivo. Clinically, high IMPA2 expression was strongly correlated with large tumor size, high grade, metastasis and poor survival, indicating poor prognosis in breast cancer patients. These findings suggest that IMPA2-mediated MI-PI cycle allows crosstalk between metabolic and oncogenic pathways to promote BLBC progression.

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