Last update 01 Nov 2024

calcium channel x ASIC1

Last update 01 Nov 2024

Basic Info

Related Targets

calcium channelASIC1

Drugs associated with calcium channel x ASIC1

NPI-506

Target

ASIC1 x calcium channel

Mechanism

ASIC1 antagonists [+1]

Active Org.-

Originator Org.

Neuroprotect, Inc.

Active Indication-

Inactive Indication

Brain Ischemia

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with calcium channel x ASIC1

100 Translational Medicine associated with calcium channel x ASIC1

0 Patents (Medical) associated with calcium channel x ASIC1

Literatures (Medical) associated with calcium channel x ASIC1

01 Apr 2014·Expert Opinion on Therapeutic TargetsQ2 · MEDICINE

Targeting cell surface trafficking of pain-facilitating receptors to treat chronic pain conditions

Q2 · MEDICINE

Review

Author: Weiya Ma ; Remi Quirion

INTRODUCTIONChronic pain conditions are serious clinical concerns. Its genesis is closely associated with sensitization of nociceptive primary sensory neurons (nociceptors) and dorsal horn neurons by various pain mediators produced during inflammation and tissue injury. Growing evidence showed that increasing cell surface trafficking of pain-facilitating receptors is an important mechanism underlying the peripheral and central sensitization.AREAS COVEREDWe summarized the progress of this area over the past decade by showing that inflammation, tissue damage or pain mediators facilitate cell surface trafficking of pain-facilitating receptors such as transient receptor potential vanilloid-1, transient receptor potential ankyrin-1, voltage-gated sodium channel 1.8, P2X3 and EP4 in primary sensory neurons, GluR1 and GluR2 of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, NR1 and NR2 of N-methyl-d-aspartate receptors and acid-sensing ion channels 1 in dorsal horn neurons and P2X4 in spinal microglia. The anti-allodynic effects of gabapentin was mediated by blocking surface trafficking of α2δ1 and α2δ2 subunits of voltage-gated calcium channels in primary sensory and dorsal horn neurons.EXPERT OPINIONPain mediators stimulate forward surface trafficking of their own and/or other pain-facilitating receptors to amplify pain intensity and duration. Enhancing surface abundance of pain-facilitating receptors in nociceptors and dorsal horn neurons is an important mechanism underpinning chronic pain states. Targeting specific trafficking events of pain-facilitating receptors may open a novel therapeutic avenue to more efficiently treat chronic pain conditions.

01 Nov 2011·British Journal of PharmacologyQ2 · MEDICINE

Sinomenine protects neurons from ischemic injury

Q2 · MEDICINE

Article

Author: Fang Wang ; Peng-Fei Wu ; Xiang-Long Chen ; Zui Zhang ; Lan Ni ; Jun Gu ; Wen-Ning Wu ; Jian-Guo Chen ; Qiu-Ju Xiong ; Yuan-Jian Yang

BACKGROUND AND PURPOSESinomenine (SN), a bioactive alkaloid, has been utilized clinically to treat rheumatoid arthritis in China. Our preliminary experiments indicated that it could protect PC12 cells from oxygen-glucose deprivation-reperfusion (OGD-R), we thus investigated the possible effects of SN on cerebral ischaemia and the related mechanism.EXPERIMENTAL APPROACHMiddle cerebral artery occlusion in rats was used as an animal model of ischaemic stroke in vivo. The mechanisms of the effects of SN were investigated in vitro using whole-cell patch-clamp recording, calcium imaging in PC12 cells and rat cortical neurons subjected to OGD-R.KEY RESULTSPretreatment with SN (10 and 30 mg·kg(-1) , i.p.) significantly decreased brain infarction and the overactivation of calcium-mediated events in rats subjected to 2 h ischaemia followed by 24 h reperfusion. Extracellular application of SN inhibited the currents mediated by acid-sensing ion channel 1a and L-type voltage-gated calcium channels, in the rat cultured neurons, in a concentration-dependent manner. These inhibitory effects contribute to the neuroprotection of SN against OGD-R and extracellular acidosis-induced cytotoxicity. More importantly, administration of SN (30 mg·kg(-1) , i.p.) at 1 and 2 h after cerebral ischaemia also decreased brain infarction and improved functional recovery.CONCLUSION AND IMPLICATIONSSN exerts potent protective effects against ischaemic brain injury when administered before ischaemia or even after the injury. The inhibitory effects of SN on acid-sensing ion channel 1a and L-type calcium channels are involved in this neuroprotection.

01 Jan 2010·Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine

[Alteration of ion channel gene expression profile in rat model of post-myocardial infarction heart failure].

Article

Author: Lou, Li-xia ; Zhang, Dong-mei ; Wu, Ai-ming

OBJECTIVETo investigate the ion channel genes related with the genesis and development of heart failure after myocardial infarction through analyzing the differential gene expressions in non-infarcted myocardial tissues of post-myocardial infarction heart failure (PIHF) rat model, and that of normal rat, and the bio-informatics Stc-GO analysis on them.METHODSRat model of PIHF was established by left anterior descending coronary artery ligation in six SD rats, and a control group with six sham-operative rats was set. Myocardial samples were taken in two batches from them (three rats in each group) at the heart failure formation stage and the stable stage (10 days and 8 weeks after operation) respectively. Total RNA extraction, probe preparation with reverse transcription, hybridization with double-channel cDNA microarray of rat's ion channel genes, and computerized differential gene expression screening were conducted, and Stc-GO functional clustering analysis was performed on the outcomes obtained to search out the GO sort of significance in them.RESULTSAt 10 days after operation, 319 common differential expressed genes were found from the 746 target genes, all of them were up-regulated. At 8 weeks after operation, in the 276 differential expressed genes, 274 were up-regulated while the other two down-regulated. The up-regulated genes were those concerning receptors of various hormones, cytokines, neuro-hormones, growth factors and nuclear receptor, protein phosphorylase, G protein, various ion channels mediated by ligand or voltage, transport protein, receptor interfering protein, etc. The down-regulated genes concerning the potassium channel and transport protein, etc. Stc-GO analysis found that the six genes concerning adrenergic receptor kinase beta 1 (betaARK1), amiloride-sensitive cation channel 2 neuronal (Accn2), voltage-dependent calcium ion channel gamma subunit 1 (Cacng1), cyclic nucleotide gated channel alpha 1 (Cnga1), Glutamate receptor ionotropic kainite 2 (Grik 2) and neurotrophic tyrosine kinase receptor type 2 (Ntrk 2), were all the significantly up-regulated differential genes of the model group related with the sham-operative group, and all showed a down-regulating trend as time goes on, and four genes in them were validated by the RT-PCR test.CONCLUSIONIon channel genes concerning Accn2, Grik2, Ntrk2 and Cacng1 were up-regulated in PIHF, and its mechanism is waiting for further study.

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