carbamates has been researched along with Nerve Pain in 23 studies
| Excerpt | Relevance | Reference |
|---|---|---|
| "The expression level of PICK1 in dorsal root ganglion (DRG) of rats was changed by vector plasmid, and the effect of PICK1 on paclitaxel (PTL)-induced neuralgia of rats was observed in collaboration with FSC231 treatment." | 8.02 | FSC231 alleviates paclitaxel-induced neuralgia by inhibiting the interactions between PICK1 and GluA2 and activates GSK-3β and ERK1/2. ( Peng, Y; Ran, R; Wang, J; Xiao, Y; Zhang, X, 2021) |
| "To explore the inhibitory effect of FSC231, a PDZ domain inhibitor of protein interacting with C kinase 1 (PICK1), on paclitaxel induced neuralgia and its possible pathways." | 8.02 | FSC231 can alleviate paclitaxel-induced neuralgia by inhibiting PICK1 and affecting related factors. ( Pan, X; Wang, G; Xiao, Y; Zhang, X, 2021) |
| "The expression level of PICK1 in dorsal root ganglion (DRG) of rats was changed by vector plasmid, and the effect of PICK1 on paclitaxel (PTL)-induced neuralgia of rats was observed in collaboration with FSC231 treatment." | 4.02 | FSC231 alleviates paclitaxel-induced neuralgia by inhibiting the interactions between PICK1 and GluA2 and activates GSK-3β and ERK1/2. ( Peng, Y; Ran, R; Wang, J; Xiao, Y; Zhang, X, 2021) |
| "To explore the inhibitory effect of FSC231, a PDZ domain inhibitor of protein interacting with C kinase 1 (PICK1), on paclitaxel induced neuralgia and its possible pathways." | 4.02 | FSC231 can alleviate paclitaxel-induced neuralgia by inhibiting PICK1 and affecting related factors. ( Pan, X; Wang, G; Xiao, Y; Zhang, X, 2021) |
| "JZL195 and the cannabinoid receptor agonist WIN55212 produced dose-dependent reductions in CCI-induced mechanical and cold allodynia, plus side effects including motor incoordination, catalepsy and sedation." | 3.83 | Actions of the dual FAAH/MAGL inhibitor JZL195 in a murine neuropathic pain model. ( Adamson Barnes, NS; Kazantzis, NP; Mitchell, VA; Vaughan, CW, 2016) |
| " administration of morphine and the selective MAGL inhibitor 2,5-dioxopyrrolidin-1-yl 4-(bis(4-chlorophenyl)methyl)piperazine-1-carboxylate (MJN110) were tested alone and in combination at equieffective doses for reversal of CCI-induced mechanical allodynia and thermal hyperalgesia." | 3.83 | The Selective Monoacylglycerol Lipase Inhibitor MJN110 Produces Opioid-Sparing Effects in a Mouse Neuropathic Pain Model. ( Abdullah, RA; Akbarali, H; Banks, ML; Cravatt, BF; Dewey, WL; Grim, TW; Lichtman, AH; Mustafa, MA; Niphakis, MJ; Poklis, JL; Wilkerson, JL; Wise, LE, 2016) |
| "The mechanisms involved in neuropathic pain are complex and involve both peripheral and central phenomena." | 2.48 | Modulation of neuropathic-pain-related behaviour by the spinal endocannabinoid/endovanilloid system. ( Przewlocka, B; Starowicz, K, 2012) |
| "Neuropathic pain is often associated with depression." | 1.51 | Inhibition of Fatty Acid Amide Hydrolase Improves Depressive-Like Behaviors Independent of Its Peripheral Antinociceptive Effects in a Rat Model of Neuropathic Pain. ( Gong, DY; Hai, KR; Jiang, HX; Ke, BW; Liu, J; Ma, G; Yang, Z; Zhou, C, 2019) |
| "Neuropathic pain was induced by chronic constriction injury (CCI) of the mouse sciatic nerve and examined by Hargreaves and Von Frey tests." | 1.48 | WWL70 protects against chronic constriction injury-induced neuropathic pain in mice by cannabinoid receptor-independent mechanisms. ( Cox, B; Jones, M; Selvaraj, P; Symes, AJ; Tanaka, M; Wen, J; Zhang, Y, 2018) |
| "Paclitaxel produced mechanical and cold allodynia without altering nestlet shredding or marble burying behaviors." | 1.48 | Brain-Permeant and -Impermeant Inhibitors of Fatty Acid Amide Hydrolase Synergize with the Opioid Analgesic Morphine to Suppress Chemotherapy-Induced Neuropathic Nociception Without Enhancing Effects of Morphine on Gastrointestinal Transit. ( Hohmann, AG; Iyer, V; Makriyannis, A; Saberi, SA; Slivicki, RA; Vemuri, VK, 2018) |
| "SA-57 dose-dependently reversed mechanical allodynia in the constriction injury (CCI) of the sciatic nerve model of neuropathic pain and carrageenan inflammatory pain model." | 1.46 | The endocannabinoid hydrolysis inhibitor SA-57: Intrinsic antinociceptive effects, augmented morphine-induced antinociception, and attenuated heroin seeking behavior in mice. ( Abdullah, RA; Cabrera, R; Cravatt, BF; Ghosh, S; Lichtman, AH; Maldonado, RL; Mustafa, M; Niphakis, MJ; Wilkerson, JL, 2017) |
| "Spinal AEA reduces neuropathic pain by acting at both cannabinoid CB1 receptors and transient receptor potential vanilloid-1 (TRPV1) channels." | 1.39 | Full inhibition of spinal FAAH leads to TRPV1-mediated analgesic effects in neuropathic rats and possible lipoxygenase-mediated remodeling of anandamide metabolism. ( Cristino, L; De Petrocellis, L; Di Marzo, V; Korostynski, M; Makuch, W; Malek, N; Petrosino, S; Przewlocka, B; Slezak, M; Starowicz, K; Zychowska, M, 2013) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 1 (4.35) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 3 (13.04) | 29.6817 |
| 2010's | 16 (69.57) | 24.3611 |
| 2020's | 3 (13.04) | 2.80 |
| Authors | Studies |
|---|---|
| Zhang, X | 2 |
| Wang, J | 1 |
| Ran, R | 1 |
| Peng, Y | 1 |
| Xiao, Y | 2 |
| Wang, G | 1 |
| Pan, X | 1 |
| Lu, R | 1 |
| Cui, SS | 1 |
| Wang, XX | 1 |
| Chen, L | 1 |
| Liu, F | 1 |
| Gao, J | 1 |
| Wang, W | 1 |
| Wen, J | 1 |
| Jones, M | 1 |
| Tanaka, M | 1 |
| Selvaraj, P | 1 |
| Symes, AJ | 1 |
| Cox, B | 1 |
| Zhang, Y | 1 |
| Jiang, HX | 1 |
| Ke, BW | 1 |
| Liu, J | 1 |
| Ma, G | 1 |
| Hai, KR | 1 |
| Gong, DY | 1 |
| Yang, Z | 1 |
| Zhou, C | 1 |
| Slivicki, RA | 2 |
| Saberi, SA | 1 |
| Iyer, V | 1 |
| Vemuri, VK | 1 |
| Makriyannis, A | 1 |
| Hohmann, AG | 2 |
| Li, L | 1 |
| Li, J | 1 |
| Zuo, Y | 1 |
| Dang, D | 1 |
| Frost, JA | 1 |
| Yang, Q | 1 |
| Xu, Z | 1 |
| Mali, SS | 1 |
| Starowicz, K | 2 |
| Makuch, W | 1 |
| Korostynski, M | 1 |
| Malek, N | 1 |
| Slezak, M | 1 |
| Zychowska, M | 1 |
| Petrosino, S | 1 |
| De Petrocellis, L | 1 |
| Cristino, L | 1 |
| Przewlocka, B | 2 |
| Di Marzo, V | 1 |
| Hama, AT | 1 |
| Germano, P | 1 |
| Varghese, MS | 1 |
| Cravatt, BF | 4 |
| Milne, GT | 1 |
| Pearson, JP | 1 |
| Sagen, J | 1 |
| Pottabathini, R | 1 |
| Kumar, A | 1 |
| Bhatnagar, A | 1 |
| Garg, S | 1 |
| Ignatowska-Jankowska, B | 1 |
| Wilkerson, JL | 3 |
| Mustafa, M | 2 |
| Abdullah, R | 1 |
| Niphakis, M | 1 |
| Wiley, JL | 1 |
| Lichtman, AH | 3 |
| Adamson Barnes, NS | 1 |
| Mitchell, VA | 2 |
| Kazantzis, NP | 1 |
| Vaughan, CW | 2 |
| Niphakis, MJ | 2 |
| Grim, TW | 1 |
| Mustafa, MA | 1 |
| Abdullah, RA | 2 |
| Poklis, JL | 1 |
| Dewey, WL | 1 |
| Akbarali, H | 1 |
| Banks, ML | 1 |
| Wise, LE | 1 |
| Bernal, L | 1 |
| Lopez-Garcia, JA | 1 |
| Roza, C | 1 |
| Ghosh, S | 1 |
| Cabrera, R | 1 |
| Maldonado, RL | 1 |
| de Biase, S | 1 |
| Merlino, G | 1 |
| Lorenzut, S | 1 |
| Valente, M | 1 |
| Gigli, GL | 1 |
| Rauck, R | 1 |
| Makumi, CW | 1 |
| Schwartz, S | 1 |
| Graff, O | 1 |
| Meno-Tetang, G | 1 |
| Bell, CF | 1 |
| Kavanagh, ST | 1 |
| McClung, CL | 1 |
| Blackburn-Munro, G | 1 |
| Jensen, BS | 1 |
| Jayamanne, A | 1 |
| Greenwood, R | 1 |
| Aslan, S | 1 |
| Piomelli, D | 1 |
| Trang, T | 1 |
| Borello, ED | 1 |
| Vago Muiños, HA | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Study PXN110448: A Dose-response Study of XP13512, Compared With Concurrent Placebo Control and LYRICA(Pregabalin), in Subjects With Neuropathic Pain Associated Withdiabetic Peripheral Neuropathy (DPN)[NCT00643760] | Phase 2 | 421 participants (Actual) | Interventional | 2008-03-31 | Completed | ||
| Genetic, Epigenetic, Psychosocial, and Biological Determinants of Post-surgical Pain After Pectus or Spine Surgery[NCT04031716] | 600 participants (Anticipated) | Interventional | 2018-07-06 | Enrolling by invitation | |||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Baseline and EOMT scores are the pain scores each participant reported after taking a 50-foot walk at the randomization and Week 13/Withdrawal visits, respectively, using an 11-point PI-NRS (0=no pain, 10=pain as bad as you can imagine). Change from baseline was calculated as the EOMT score minus the baseline score. An ANCOVA model with BMI, baseline pain intensity after 50-foot walk, pain intensity prior to 50-foot walk at the visit being assessed, and grouped center as covariates was used. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) |
|---|---|
| Placebo | -2.38 |
| GEn 1200 mg/Day | -2.32 |
| GEn 2400 mg/Day | -2.36 |
| GEn 3600 mg/Day | -2.52 |
| PGB 300 mg/Day | -2.17 |
Baseline and EOMT values are the calculated means of the daily 24-hour API scores for each participant during the last 7 days prior to randomization (Baseline) and the earliest date of Week 13 visit/Withdrawal visit/last dose of study drug (EOMT). Participants used a hand-held diary to rate their API over the preceding 24 hours, using an 11-point Pain Intensity Numerical Rating Scale (PI-NRS) (0=no pain, 10=pain as bad as you can imagine). LOCF was used if less than 4 days of diary data were provided. Change from baseline was calculated as the EOMT score minus the Baseline score. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) |
|---|---|
| Placebo | -2.08 |
| GEn 1200 mg/Day | -2.43 |
| GEn 2400 mg/Day | -2.10 |
| GEn 3600 mg/Day | -2.63 |
| PGB 300 mg/Day | -1.65 |
"Current pain is defined as the participant's assessment of pain intensity right now. Participants recorded their current evening pain intensity in the evening before bedtime using an 11-point PI-NRS (0=no pain, 10=pain as bad as you can imagine). Baseline and EOMT are as defined for the primary endpoint. Change from baseline was calculated as the EOMT score minus the baseline score. An ANCOVA model with baseline value, BMI, grouped center as covariates was used." (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) |
|---|---|
| Placebo | -2.19 |
| GEn 1200 mg/Day | -2.24 |
| GEn 2400 mg/Day | -2.10 |
| GEn 3600 mg/Day | -2.66 |
| PGB 300 mg/Day | -1.65 |
"Current pain is defined as the participant's assessment of pain intensity right now. Participants recorded their current morning pain intensity in the morning upon wakening using an 11-point PI-NRS (0=no pain, 10=pain as bad as you can imagine). Baseline and EOMT are as defined for the primary endpoint. Change from baseline was calculated as the EOMT score minus the baseline score. An ANCOVA model with baseline value, BMI, grouped center as covariates was used." (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) |
|---|---|
| Placebo | -1.90 |
| GEn 1200 mg/Day | -2.08 |
| GEn 2400 mg/Day | -1.95 |
| GEn 3600 mg/Day | -2.40 |
| PGB 300 mg/Day | -1.50 |
Mean daily use of rescue medication (milligrams of acetaminophen) was calculated by determining the average number of tablets taken per day of rescue medication (Commerical Tylenol) during treatment and multiplying that by 500 mg. Baseline and EOMT are as defined for the primary endpoint. Change from baseline was calculated as the EOMT score minus the baseline score. An ANCOVA model with baseline value, BMI, grouped center as covariates was used. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | milligrams (Least Squares Mean) |
|---|---|
| Placebo | -261.99 |
| GEn 1200 mg/Day | -171.64 |
| GEn 2400 mg/Day | -102.51 |
| GEn 3600 mg/Day | -228.54 |
| PGB 300 mg/Day | -246.07 |
Day-time is defined as the time between rising in the morning and going to bed at night. Participants recorded day-time API on a daily basis in the evening before bedtime using an 11-point PI-NRS (0=no pain, 10=pain as bad as you can imagine). Baseline and EOMT are as defined for the primary endpoint. Change from baseline was calculated as the EOMT score minus the baseline score. An ANCOVA model with baseline value, BMI, grouped center as covariates was used. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) |
|---|---|
| Placebo | -2.07 |
| GEn 1200 mg/Day | -2.35 |
| GEn 2400 mg/Day | -2.06 |
| GEn 3600 mg/Day | -2.54 |
| PGB 300 mg/Day | -1.50 |
Day-time worst pain is defined as the partipant's assessment of their worst pain between rising in the morning and going to bed at night. Participants recorded day-time worst pain in the evening before bedtime using an 11-point PI-NRS (0=no pain, 10=pain as bad as you can imagine). Baseline and EOMT are as defined for the primary endpoint. Change from baseline was calculated as the EOMT score minus the baseline score. An ANCOVA model with baseline value, BMI, grouped center as covariates was used. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) |
|---|---|
| Placebo | -2.33 |
| GEn 1200 mg/Day | -2.35 |
| GEn 2400 mg/Day | -2.25 |
| GEn 3600 mg/Day | -2.88 |
| PGB 300 mg/Day | -1.62 |
Night-time is defined as the time between going to bed at night and rising in the morning. Participants recorded night-time API on a daily basis in the morning upon awakening using an 11-point PI-NRS (0=no pain, 10=pain as bad as you can imagine). Baseline and EOMT are as defined for the primary endpoint. Change from baseline was calculated as the EOMT score minus the baseline score. An ANCOVA model with baseline value, BMI, grouped center as covariates was used. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) |
|---|---|
| Placebo | -1.99 |
| GEn 1200 mg/Day | -2.15 |
| GEn 2400 mg/Day | -2.04 |
| GEn 3600 mg/Day | -2.71 |
| PGB 300 mg/Day | -1.83 |
Night-time worst pain is defined as the partipant's assessment of their worst pain between going to bed at night and rising in the morning. Participants recorded night-time worst pain in the morning upon awakening using an 11-point PI-NRS (0=no pain, 10=pain as bad as you can imagine). Baseline and EOMT are as defined for the primary endpoint. Change from baseline was calculated as the EOMT score minus the baseline score. An ANCOVA model with baseline value, BMI, grouped center as covariates was used. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) |
|---|---|
| Placebo | -2.25 |
| GEn 1200 mg/Day | -2.24 |
| GEn 2400 mg/Day | -2.25 |
| GEn 3600 mg/Day | -3.00 |
| PGB 300 mg/Day | -1.86 |
Participants assessed sleep interference due to pain on a daily basis in the morning upon awakening using an 11-point NRS (0=pain does not interfere with sleep, 10=pain completely interferes with sleep). Baseline and EOMT are as defined for the primary endpoint. Change from baseline was calculated as the EOMT score minus the baseline score. An ANCOVA model with baseline value, BMI, grouped center as covariates was used. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) |
|---|---|
| Placebo | -2.35 |
| GEn 1200 mg/Day | -2.54 |
| GEn 2400 mg/Day | -2.45 |
| GEn 3600 mg/Day | -3.01 |
| PGB 300 mg/Day | -2.24 |
"The CGIC is a single-item questionnaire designed to provide an overall assessment of treatment from the clinician's perspective since the start of the study. It is measured on a 7-point scale, where 1=very much improved and 7=very much worse. A participant is considered a responder if they have a response of very much improved or much improved. EOMT response is defined as the score recorded at the Week 13/Withdrawal visit." (NCT00643760)
Timeframe: EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | participants (Number) |
|---|---|
| Placebo | 39 |
| GEn 1200 mg/Day | 20 |
| GEn 2400 mg/Day | 22 |
| GEn 3600 mg/Day | 50 |
| PGB 300 mg/Day | 17 |
"The PGIC is a single-item questionnaire designed to provide an overall assessment of treatment from the participant's perspective since the start of the study. It is measured on a 7-point scale, where 1=very much improved and 7=very much worse. A participant is considered a responder if they have a response of very much improved or much improved. EOMT response is defined as the score recorded at the Week 13/Withdrawal visit." (NCT00643760)
Timeframe: EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | participants (Number) |
|---|---|
| Placebo | 46 |
| GEn 1200 mg/Day | 22 |
| GEn 2400 mg/Day | 24 |
| GEn 3600 mg/Day | 53 |
| PGB 300 mg/Day | 62 |
Sustained improvement in the 24-hour average pain intensity score is defined as at least 2 consecutive days on which the 24-hour average pain intensity score is >=2 points less than the mean 24-hour average pain intensity score at baseline. Time to onset is measured from baseline and was calculated as first day of event minus last day of baseline and is expressed in days. Baseline score is the calculated mean of the 24-hour average pain score for each participant during the last 7 days prior to randomization. (NCT00643760)
Timeframe: Any time post-baseline until date of last dose of study medication (up to Week 13)
| Intervention | days (Median) |
|---|---|
| Placebo | 24 |
| GEn 1200 mg/Day | 25 |
| GEn 2400 mg/Day | 22 |
| GEn 3600 mg/Day | 15 |
| PGB 300 mg/Day | 29 |
The POMS-B, an emotional functioning instrument, assesses mood, tension, and other psychological symptoms and consists of 30-items assessed on a 5-point scale (0=not at all to 4=extremely). 6 summary scores are calculated: Tension/Anxiety, Depression/Rejection, Anger/Hostility, Vigor/Activity, Fatigue/Inertia, and Confusion/Bewilderment; and range from 0-20 (higher scores = more negative mood state). Analysis of this endpoint is based on the change from baseline (BL) (EOMT score minus the BL score) using an ANCOVA model with BL value, BMI, grouped center as covariates. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) | |||||
|---|---|---|---|---|---|---|
| Tension/Anxiety Domain Score | Depression/Rejection Domain Score | Anger/Hostility Domain Score | Vigor/Activity Domain Score | Fatigue/Inertia Domain Score | Confusion/Bewilderment Domain Score | |
| GEn 1200 mg/Day | -0.6 | -0.2 | -0.8 | -0.1 | -0.5 | 0.2 |
| GEn 2400 mg/Day | -0.7 | -0.6 | -0.5 | 0.1 | -1.1 | -0.1 |
| GEn 3600 mg/Day | -0.9 | -0.3 | -0.3 | 0.7 | -1.1 | 0.0 |
| PGB 300 mg/Day | -0.3 | 0.4 | -0.3 | -0.4 | -0.1 | -0.2 |
| Placebo | -1.0 | -0.5 | -0.5 | 0.6 | -0.8 | -0.3 |
The SF-MPQ, a general pain instrument, assesses the characteristics and intensity of pain and consists of 15-items assessed on a 4-point scale (0=none, 1=mild, 2=moderate, and 3=severe). 3 summary scores are calculated: sensory score (sum of items 1-11, range 0-33), affective score (sum of items 12-15, range 0-12), total score (sum of items 1-15, range 0-45), where lower scores = lower pain/impact. Analysis is based on the change from baseline (BL) (EOMT score minus the BL score) using an ANCOVA model with BL value, BMI, grouped center as covariates. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) | ||
|---|---|---|---|
| SF-MPQ Total Score | SF-MPQ Sensory Score | SF-MPQ Affective Score | |
| GEn 1200 mg/Day | -6.55 | -4.83 | -1.65 |
| GEn 2400 mg/Day | -6.75 | -5.31 | -1.45 |
| GEn 3600 mg/Day | -7.56 | -5.50 | -2.07 |
| PGB 300 mg/Day | -4.01 | -2.73 | -1.26 |
| Placebo | -5.85 | -4.25 | -1.63 |
The NPS assesses pain qualities and consists of 11-items, 10 assessed on an 11-point NRS (0=no impact to 10=greatest impact); and 1 open-ended question not used in score calculation. 4 summary scores are calculated: NPS 10 (items 1-7, 9-11), NPS 8 (8 pain descriptor items), NPS Non-Allodynic (NA) (8 NA items), and NPS 4 (4 pain quality items); and range from 0 to 100 (0=no impact and 100=greatest impact). The analysis is based on the change from baseline (BL) (EOMT score minus the BL score) using an ANCOVA model with BL value, BMI, grouped center as covariates. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) | |||
|---|---|---|---|---|
| NPS 10 Score | NPS 8 Score | NPS Non-Allodynic Score | NPS 4 Score | |
| GEn 1200 mg/Day | -18.43 | -17.83 | -18.89 | -20.90 |
| GEn 2400 mg/Day | -22.24 | -21.84 | -22.86 | -25.15 |
| GEn 3600 mg/Day | -25.49 | -25.14 | -26.35 | -27.84 |
| PGB 300 mg/Day | -16.16 | -16.19 | -15.63 | -16.06 |
| Placebo | -18.92 | -18.73 | -19.37 | -20.54 |
The SF-36 is a general health-related quality of life instrument consisting of 36 items with various response options (Yes/No, 5- to 6-point Likert scale). Summary scores are calculated for 8 domains and 2 components (physical and mental); where scores range from 0 to 100 (higher scores = better quality of life). Analysis of this endpoint is based on the change from baseline (BL) (EOMT score minus the BL score) using an ANCOVA model with BL value, BMI, grouped center as covariates. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | scores on a scale (Least Squares Mean) | |
|---|---|---|
| SF-36 Physical Component Summary Score | SF-36 Mental Component Summary Score | |
| GEn 1200 mg/Day | 3.5 | 0.4 |
| GEn 2400 mg/Day | 3.7 | 1.5 |
| GEn 3600 mg/Day | 4.6 | 1.6 |
| PGB 300 mg/Day | 3.7 | 0.7 |
| Placebo | 3.1 | 2.5 |
The BPI, a general pain instrument, assesses the severity and interference of pain; and consists of 6 items assessed on an 11-point NRS (0=no impact and 10=greatest impact). 2 summary scores are calculated: BPI Severity Score (average of first 4 items) and BPI Interference Score (average of 7 responses to item 6); where each summary score ranges from 0 to 10 (0=no impact and 10=greatest impact). Analysis of this endpoint is based on the change from baseline (BL) (EOMT score minus the BL score) using an ANCOVA model with BL value, BMI, grouped center as covariates. (NCT00643760)
Timeframe: Baseline and EOMT
| Intervention | scores on a scale (Least Squares Mean) | |
|---|---|---|
| Brief Pain Inventory Severity of Pain | Brief Pain Inventory Interference of Pain | |
| GEn 1200 mg/Day | -2.3 | -2.0 |
| GEn 2400 mg/Day | -2.4 | -2.1 |
| GEn 3600 mg/Day | -2.8 | -2.5 |
| PGB 300 mg/Day | -1.7 | -1.9 |
| Placebo | -2.1 | -2.0 |
Baseline and EOMT scores are the calculated means of the 24-hour average pain scores for each participant during the last 7 days prior to randomization and EOMT, respectively. Percent reduction from baseline was calculated as the [(EOMT score minus the baseline score)divided by the baseline score], multiplied by 100. The PI-NRS is an 11-point scale (0=no pain, 10=pain as bad as you can imagine) by which a participant assesses their 24-hour average pain intensity. (NCT00643760)
Timeframe: Baseline and EOMT (representing the earliest date of Week 13 visit/withdrawal visit)
| Intervention | participants (Number) | ||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| >= 0% reduction from baseline | >= 10% reduction from baseline | >= 20% reduction from baseline | >= 30% reduction from baseline | >= 40% reduction from baseline | >= 50% reduction from baseline | >= 60% reduction from baseline | >= 70% reduction from baseline | >= 80% reduction from baseline | >= 90% reduction from baseline | 100% reduction from baseline | |
| GEn 1200 mg/Day | 55 | 43 | 36 | 31 | 28 | 26 | 21 | 17 | 11 | 5 | 4 |
| GEn 2400 mg/Day | 50 | 42 | 34 | 25 | 19 | 15 | 11 | 6 | 5 | 2 | 1 |
| GEn 3600 mg/Day | 101 | 91 | 78 | 66 | 55 | 46 | 41 | 25 | 17 | 8 | 5 |
| PGB 300 mg/Day | 55 | 42 | 36 | 28 | 20 | 14 | 9 | 5 | 4 | 3 | 3 |
| Placebo | 103 | 86 | 73 | 57 | 46 | 35 | 26 | 15 | 11 | 4 | 3 |
3 reviews available for carbamates and Nerve Pain
| Article | Year |
|---|---|
ADMET considerations for restless leg syndrome drug treatments.
Topics: Amines; Anticonvulsants; Benzothiazoles; Carbamates; Cyclohexanecarboxylic Acids; Dopamine Agents; D | 2012 |
Modulation of neuropathic-pain-related behaviour by the spinal endocannabinoid/endovanilloid system.
Topics: Amides; Amidohydrolases; Animals; Arachidonic Acid; Arachidonic Acids; Behavior; Benzamides; Carbama | 2012 |
Inhibition of fatty acid amide hydrolase: a potential treatment for neuropathic pain.
Topics: Amidohydrolases; Animals; Benzamides; Carbamates; Mice; Neuralgia; Rats | 2007 |
1 trial available for carbamates and Nerve Pain
| Article | Year |
|---|---|
A randomized, controlled trial of gabapentin enacarbil in subjects with neuropathic pain associated with diabetic peripheral neuropathy.
Topics: Adult; Aged; Aged, 80 and over; Carbamates; Diabetic Neuropathies; Dose-Response Relationship, Drug; | 2013 |
19 other studies available for carbamates and Nerve Pain
| Article | Year |
|---|---|
FSC231 alleviates paclitaxel-induced neuralgia by inhibiting the interactions between PICK1 and GluA2 and activates GSK-3β and ERK1/2.
Topics: Animals; Carbamates; Cinnamates; Glycogen Synthase Kinase 3 beta; Neuralgia; Paclitaxel; Rats | 2021 |
FSC231 can alleviate paclitaxel-induced neuralgia by inhibiting PICK1 and affecting related factors.
Topics: Analgesics; Animals; Carbamates; Cell Cycle Proteins; Cinnamates; Ganglia, Spinal; Inflammation Medi | 2021 |
Astrocytic c-Jun N-terminal kinase-histone deacetylase-2 cascade contributes to glutamate transporter-1 decrease and mechanical allodynia following peripheral nerve injury in rats.
Topics: Animals; Anthracenes; Astrocytes; Carbamates; Cells, Cultured; Etanercept; Excitatory Amino Acid Tra | 2021 |
WWL70 protects against chronic constriction injury-induced neuropathic pain in mice by cannabinoid receptor-independent mechanisms.
Topics: Animals; Biphenyl Compounds; Cannabinoid Receptor Agonists; Cannabinoid Receptor Antagonists; Carbam | 2018 |
Inhibition of Fatty Acid Amide Hydrolase Improves Depressive-Like Behaviors Independent of Its Peripheral Antinociceptive Effects in a Rat Model of Neuropathic Pain.
Topics: Amidohydrolases; Animals; Arachidonic Acids; Behavior, Animal; Benzamides; Carbamates; Depression; D | 2019 |
Brain-Permeant and -Impermeant Inhibitors of Fatty Acid Amide Hydrolase Synergize with the Opioid Analgesic Morphine to Suppress Chemotherapy-Induced Neuropathic Nociception Without Enhancing Effects of Morphine on Gastrointestinal Transit.
Topics: Amidohydrolases; Analgesics, Opioid; Animals; Antineoplastic Agents; Arachidonic Acids; Benzamides; | 2018 |
Activation of KCNQ Channels Prevents Paclitaxel-Induced Peripheral Neuropathy and Associated Neuropathic Pain.
Topics: Animals; Antineoplastic Agents, Phytogenic; Breast Neoplasms; Carbamates; Cell Line, Tumor; Drug Rep | 2019 |
Brain permeant and impermeant inhibitors of fatty-acid amide hydrolase suppress the development and maintenance of paclitaxel-induced neuropathic pain without producing tolerance or physical dependence in vivo and synergize with paclitaxel to reduce tumor
Topics: Amidohydrolases; Analgesics; Animals; Antineoplastic Agents; Benzamides; Benzoxazines; Brain; Cannab | 2019 |
Full inhibition of spinal FAAH leads to TRPV1-mediated analgesic effects in neuropathic rats and possible lipoxygenase-mediated remodeling of anandamide metabolism.
Topics: Amides; Amidohydrolases; Analgesia; Animals; Arachidonate 15-Lipoxygenase; Arachidonic Acids; Benzam | 2013 |
Fatty acid amide hydrolase (FAAH) inhibitors exert pharmacological effects, but lack antinociceptive efficacy in rats with neuropathic spinal cord injury pain.
Topics: Amidohydrolases; Analgesics; Animals; Arachidonic Acids; Benzamides; Benzoxazines; Brain; Carbamates | 2014 |
Possible involvement of nitric oxide modulatory mechanism in the protective effect of retigabine against spinal nerve ligation-induced neuropathic pain.
Topics: Animals; Carbamates; Ligation; Male; Neuralgia; Neuroprotective Agents; Nitric Oxide; Pain Threshold | 2015 |
Selective monoacylglycerol lipase inhibitors: antinociceptive versus cannabimimetic effects in mice.
Topics: Analgesics; Animals; Benzodioxoles; Biomimetic Materials; Brain; Cannabinoids; Carbamates; Constrict | 2015 |
Actions of the dual FAAH/MAGL inhibitor JZL195 in a murine neuropathic pain model.
Topics: Amidohydrolases; Animals; Benzamides; Benzodioxoles; Benzoxazines; Carbamates; Disease Models, Anima | 2016 |
The Selective Monoacylglycerol Lipase Inhibitor MJN110 Produces Opioid-Sparing Effects in a Mouse Neuropathic Pain Model.
Topics: Analgesics, Opioid; Animals; Arachidonic Acids; Behavior, Animal; Carbamates; Constriction, Patholog | 2016 |
Spontaneous activity in C-fibres after partial damage to the saphenous nerve in mice: Effects of retigabine.
Topics: Action Potentials; Animals; Axotomy; Carbamates; Disease Models, Animal; Male; Membrane Transport Mo | 2016 |
The endocannabinoid hydrolysis inhibitor SA-57: Intrinsic antinociceptive effects, augmented morphine-induced antinociception, and attenuated heroin seeking behavior in mice.
Topics: Acetamides; Analgesics; Analgesics, Opioid; Animals; Arachidonic Acid; Arachidonic Acids; Carbamates | 2017 |
The anticonvulsant retigabine attenuates nociceptive behaviours in rat models of persistent and neuropathic pain.
Topics: Animals; Anthracenes; Anticonvulsants; Behavior, Animal; Carbamates; Disease Models, Animal; Dose-Re | 2003 |
Actions of the FAAH inhibitor URB597 in neuropathic and inflammatory chronic pain models.
Topics: Amidohydrolases; Animals; Benzamides; Carbamates; Chronic Disease; Disease Models, Animal; Enzyme In | 2006 |
[Glossopharyngeal neuralgia. A case of this rare condition treated successfully wtih 5-carbamoil diazepine].
Topics: Carbamates; Diazepam; Glossopharyngeal Nerve; Humans; Neuralgia | 1974 |