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Last update 23 Jan 2025

Opioid receptors x SCNA x μ opioid receptor

Last update 23 Jan 2025

Basic Info

Related Targets

Opioid receptorsSCNAμ opioid receptor

Drugs associated with Opioid receptors x SCNA x μ opioid receptor

Bupivacaine Hydrochloride/Fentanyl Citrate

Target

SCNA x μ opioid receptor

Mechanism

SCNA blockers [+1]

Active Org.

Amco Inc.

Originator Org.

Amco Inc.

Active Indication

Pain

Inactive Indication-

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

United Kingdom

First Approval Date01 Jan 2012

Lidocaine/Morphine

Target

Opioid receptors x SCNA x μ opioid receptor

Mechanism

Opioid receptors agonists [+2]

Active Org.-

Originator Org.

Memorial Sloan Kettering Cancer Center

Active Indication-

Inactive Indication

Pain

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with Opioid receptors x SCNA x μ opioid receptor

CTRI/2023/08/056421

/ Not yet recruitingPhase 1/2IIT

Efficacy of intrathecal 0.5% Bupivacaine with fentanyl & 0.5% Bupivacaine with Butorphanol in lower limb surgeries - Nil

Start Date26 Aug 2023

Sponsor / Collaborator-

CTRI/2023/07/055401

/ Not yet recruitingNot ApplicableIIT

Comparison of effects of epidural infusion with 0.125% Ropivacaine and Bupivacaine with Fentanyl for post operative analgesia in abdominal surgeries .A prospective randomised double blind study.

Start Date27 Jul 2023

Sponsor / Collaborator-

100 Clinical Results associated with Opioid receptors x SCNA x μ opioid receptor

100 Translational Medicine associated with Opioid receptors x SCNA x μ opioid receptor

0 Patents (Medical) associated with Opioid receptors x SCNA x μ opioid receptor

Literatures (Medical) associated with Opioid receptors x SCNA x μ opioid receptor

01 Jan 2023·Journal of Endodontics

Association Between Single-nucleotide Polymorphisms in Candidate Genes and Success of Pulpal Anesthesia after Inferior Alveolar Nerve Block

Article

Author: Kahraman, Çiğdem Y ; Karataş, Ertuğrul ; Çakmak, Fatma A ; Sümbüllü, Meltem

INTRODUCTIONThe present study aimed to investigate the possible association between the single-nucleotide polymorphisms (SNPs) in the SCN9A, SCN10A, SCN11A, OPRM1, and COMT genes and the success rate of pulpal anesthesia after inferior alveolar nerve block (IANB).METHODSA total of 70 patients (45 females and 25 males) presenting mandibular molar teeth with symptomatic irreversible pulpitis were included. Saliva samples were collected from the participants before the application of IANB. A standard IANB was performed with 1.8 mL 4% articaine with 1:100,000 epinephrine. Endodontic treatment was initiated 15 minutes after injection, and the patients were asked to report their pain level during the procedure on a 170-mm Heft-Parker visual analog scale. If the patient recorded a pain level of lower than 54 on the visual analog scale (no pain or mild pain), the anesthesia was considered successful. The DNA isolation and genotyping were performed, and the association between rs4286289, rs6746030, rs6795970, rs6801957, rs11709492, rs1799971, rs1799973, rs4680, rs6269, rs4633, and rs740603 SNPs and the success rate of anesthesia was investigated.RESULTSThe anesthesia success rate was significantly lower for the GG genotypes (45%) than the GA and AA genotypes (90%) for rs6795970 in the SCN10A gene. Additionally, the A allele for rs6795970 and the T allele for rs6801957 in the SCN10A gene were significantly associated with higher anesthesia success rates.CONCLUSIONSSNPs in the SCN10A gene affect the success rate of pulpal anesthesia after IANB.

03 Aug 2022·RheumatologyQ2 · MEDICINE

Interplay between genetics and lifestyle on pain susceptibility in women with fibromyalgia: the al-Ándalus project

Q2 · MEDICINE

Article

Author: Martínez-González, Luis J ; Geenen, Rinie ; Álvarez-Gallardo, Inmaculada C ; Aparicio, Virginia A ; Álvarez-Cubero, María J ; Gavilán-Carrera, Blanca ; Guerrero-González, Juan M ; Ruiz, Jonatan R ; Estévez-López, Fernando ; Camiletti-Moirón, Daniel ; Segura-Jiménez, Víctor ; Soriano-Maldonado, Alberto ; Acosta-Manzano, Pedro ; Delgado-Fernández, Manuel ; Salazar-Tortosa, Diego

AbstractObjectivesIt is widely acknowledged that the experience of pain is promoted by both genetic susceptibility and environmental factors such as engaging in physical activity (PA), and that pain-related cognitions are also important. Thus, the purpose of the present study was to test the association of 64 polymorphisms (34 candidate genes) and the gene–gene, gene–PA and gene–sedentary behaviour interactions with pain and pain-related cognitions in women with FM.MethodsSaliva samples from 274 women with FM [mean (s.d.) age 51.7 (7.7) years] were collected for extracting DNA. We measured PA and sedentary behaviour by accelerometers for a week, pain with algometry and questionnaires, and pain-related cognitions with questionnaires. To assess the robustness of the results, a meta-analysis was also performed.ResultsThe rs6311 and rs6313 polymorphisms (5-hydroxytryptamine receptor 2A, HTR2A) were individually related to algometer scores. The interaction of rs4818 (catechol-O-methyltransferase, COMT) and rs1799971 (opioid receptor μ gene, OPRM1) was related to pain catastrophizing. Five gene–behaviour interactions were significant: the interactions of sedentary behaviour with rs1383914 (adrenoceptor alpha 1A, ADRA1A), rs6860 (charged multivesicular body protein 1A, CHMP1A), rs4680 (COMT), rs165599 (COMT) and rs12994338 (SCN9A) on bodily pain subscale of the Short Form 36. Furthermore, the meta-analysis showed an association between rs4680 (COMT) and severity of FM symptoms (codominant model, P-value 0.032).ConclusionThe HTR2A gene (individually), COMT and OPRM1 gene–gene interaction, and the interactions of sedentary behaviour with ADRA1A, CHMP1A, COMT and SCN9A genes were associated with pain-related outcomes. Collectively, findings from the present study indicate a modest contribution of genetics and gene–sedentary behaviour interaction to pain and pain catastrophizing in women with FM. Future research should examine whether reducing sedentary behaviour is particularly beneficial for reducing pain in women with genetic susceptibility to pain.

17 Jul 2020·Inflammatory Bowel DiseasesQ2 · MEDICINE

Characterizing Clinical Features and Creating a Gene Expression Profile Associated With Pain Burden in Children With Inflammatory Bowel Disease

Q2 · MEDICINE

Article

Author: Knight, Brittany E ; Hyams, Jeffrey S ; Glidden, Nicole C ; Young, Erin E ; Grossi, Victoria

AbstractBackgroundThere is often dissociation between inflammatory activity and abdominal pain in children with inflammatory bowel disease (IBD), suggesting other factors may play a role in the pain experience.MethodsPatients (8 to 17 years) newly diagnosed with IBD were enrolled in the ALLAY Study: Assessing Risk Factors for Abdominal Pain in Children with Inflammatory Bowel Disease (NCT02984059). At diagnostic colonoscopy, 3 rectal biopsies were collected, and gene expression analysis was performed using Qiagen RT2 Profiler Neuropathic and Inflammatory Pain PCR Array. Relative fold difference in gene expression for 84 pain-associated genes was calculated using the 2-ΔΔ Cq method compared with pain-free controls. Factors affecting pain burden (Pain Burden Interview; PBI) were analyzed, including age, sex, rectal inflammation, and gene expression. Data were analyzed using multiple stepwise linear regression and 2-tailed t tests (P ≤ 0.05).ResultsThirty-nine newly diagnosed IBD patients were included (65% male, mean age 12.75 years [SD 2.63], 23 Crohn’s disease, 16 ulcerative colitis), along with 3 controls. Mean PBI score was 7.73 (SD 6.4, range 0 to 23) for all patients. Age and sex were not predictive of pain burden, but disease activity score was (P = 0.03). Expression of TRPV3, OPRM1, P2X3, SCN9A, PTGS2, and MAPK14 were associated with PBI score. Subsequent 2-tailed t tests comparing patients with no pain (PBI score ≦ 2, N = 11) to those with pain (PBI > 2, N = 28) confirmed differential expression of TRPV3, PTGS2, and MAPK14 was in patients with pain (all P < 0.05).ConclusionPain burden in newly diagnosed IBD patients may be linked to TRPV3, PTGS2, and MAPK14 expression, suggesting potential therapeutic targets for managing pain in IBD.

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