Page last updated: 2024-10-16

carbamates and Nerve Pain

carbamates has been researched along with Nerve Pain in 23 studies

Research Excerpts

ExcerptRelevanceReference
"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."8.02FSC231 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."8.02FSC231 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."4.02FSC231 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."4.02FSC231 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."3.83Actions 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."3.83The 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."2.48Modulation of neuropathic-pain-related behaviour by the spinal endocannabinoid/endovanilloid system. ( Przewlocka, B; Starowicz, K, 2012)
"Neuropathic pain is often associated with depression."1.51Inhibition 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."1.48WWL70 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."1.48Brain-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."1.46The 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."1.39Full 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)

Research

Studies (23)

TimeframeStudies, this research(%)All Research%
pre-19901 (4.35)18.7374
1990's0 (0.00)18.2507
2000's3 (13.04)29.6817
2010's16 (69.57)24.3611
2020's3 (13.04)2.80

Authors

AuthorsStudies
Zhang, X2
Wang, J1
Ran, R1
Peng, Y1
Xiao, Y2
Wang, G1
Pan, X1
Lu, R1
Cui, SS1
Wang, XX1
Chen, L1
Liu, F1
Gao, J1
Wang, W1
Wen, J1
Jones, M1
Tanaka, M1
Selvaraj, P1
Symes, AJ1
Cox, B1
Zhang, Y1
Jiang, HX1
Ke, BW1
Liu, J1
Ma, G1
Hai, KR1
Gong, DY1
Yang, Z1
Zhou, C1
Slivicki, RA2
Saberi, SA1
Iyer, V1
Vemuri, VK1
Makriyannis, A1
Hohmann, AG2
Li, L1
Li, J1
Zuo, Y1
Dang, D1
Frost, JA1
Yang, Q1
Xu, Z1
Mali, SS1
Starowicz, K2
Makuch, W1
Korostynski, M1
Malek, N1
Slezak, M1
Zychowska, M1
Petrosino, S1
De Petrocellis, L1
Cristino, L1
Przewlocka, B2
Di Marzo, V1
Hama, AT1
Germano, P1
Varghese, MS1
Cravatt, BF4
Milne, GT1
Pearson, JP1
Sagen, J1
Pottabathini, R1
Kumar, A1
Bhatnagar, A1
Garg, S1
Ignatowska-Jankowska, B1
Wilkerson, JL3
Mustafa, M2
Abdullah, R1
Niphakis, M1
Wiley, JL1
Lichtman, AH3
Adamson Barnes, NS1
Mitchell, VA2
Kazantzis, NP1
Vaughan, CW2
Niphakis, MJ2
Grim, TW1
Mustafa, MA1
Abdullah, RA2
Poklis, JL1
Dewey, WL1
Akbarali, H1
Banks, ML1
Wise, LE1
Bernal, L1
Lopez-Garcia, JA1
Roza, C1
Ghosh, S1
Cabrera, R1
Maldonado, RL1
de Biase, S1
Merlino, G1
Lorenzut, S1
Valente, M1
Gigli, GL1
Rauck, R1
Makumi, CW1
Schwartz, S1
Graff, O1
Meno-Tetang, G1
Bell, CF1
Kavanagh, ST1
McClung, CL1
Blackburn-Munro, G1
Jensen, BS1
Jayamanne, A1
Greenwood, R1
Aslan, S1
Piomelli, D1
Trang, T1
Borello, ED1
Vago Muiños, HA1

Clinical Trials (2)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
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 2421 participants (Actual)Interventional2008-03-31Completed
Genetic, Epigenetic, Psychosocial, and Biological Determinants of Post-surgical Pain After Pectus or Spine Surgery[NCT04031716]600 participants (Anticipated)Interventional2018-07-06Enrolling by invitation
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Change From Baseline in Pain Score After Taking a 50-foot Walk at EOMT

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)

Interventionscores 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

Change From Baseline in the Mean 24-hour Average Pain Intensity (API) Score at End of Maintenance Treatment (EOMT) Using Last Observation Carried Forward (LOCF) Data

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)

Interventionscores 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

Change From Baseline in the Mean Current (Evening) Pain Intensity Score at EOMT Using LOCF Data

"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)

Interventionscores 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

Change From Baseline in the Mean Current (Morning) Pain Intensity Score at EOMT Using LOCF Data

"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)

Interventionscores 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

Change From Baseline in the Mean Daily Dose of Rescue Medication at EOMT Using LOCF Data

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)

Interventionmilligrams (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

Change From Baseline in the Mean Day-time Average Pain Intensity (API) Score at EOMT Using LOCF Data

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)

Interventionscores 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

Change From Baseline in the Mean Day-time Worst Pain Intensity Score at EOMT Using LOCF Data

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)

Interventionscores 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

Change From Baseline in the Mean Night-time Average Pain Intensity (API) Score at EOMT Using LOCF Data

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)

Interventionscores 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

Change From Baseline in the Mean Night-time Worst Pain Intensity Score at EOMT Using LOCF Data

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)

Interventionscores 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

Change From Baseline in the Mean Sleep Interference Score at EOMT Using LOCF Data

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)

Interventionscores 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

Number of Participants Who Are Responders on the Clinician Global Impression of Change (CGIC) Questionnaire at EOMT Using LOCF Data

"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)

Interventionparticipants (Number)
Placebo39
GEn 1200 mg/Day20
GEn 2400 mg/Day22
GEn 3600 mg/Day50
PGB 300 mg/Day17

Number of Participants Who Are Responders on the Patient Global Impression of Change (PGIC) Questionnaire at EOMT Using LOCF Data

"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)

Interventionparticipants (Number)
Placebo46
GEn 1200 mg/Day22
GEn 2400 mg/Day24
GEn 3600 mg/Day53
PGB 300 mg/Day62

Time to Onset of Sustained Improvement in the 24-hour Average Pain Intensity Score

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)

Interventiondays (Median)
Placebo24
GEn 1200 mg/Day25
GEn 2400 mg/Day22
GEn 3600 mg/Day15
PGB 300 mg/Day29

Change From Baseline in Emotional Functioning as Assessed by the Profile of Mood States-Brief Form (POMS-B) at EOMT Using LOCF Data

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)

,,,,
Interventionscores on a scale (Least Squares Mean)
Tension/Anxiety Domain ScoreDepression/Rejection Domain ScoreAnger/Hostility Domain ScoreVigor/Activity Domain ScoreFatigue/Inertia Domain ScoreConfusion/Bewilderment Domain Score
GEn 1200 mg/Day-0.6-0.2-0.8-0.1-0.50.2
GEn 2400 mg/Day-0.7-0.6-0.50.1-1.1-0.1
GEn 3600 mg/Day-0.9-0.3-0.30.7-1.10.0
PGB 300 mg/Day-0.30.4-0.3-0.4-0.1-0.2
Placebo-1.0-0.5-0.50.6-0.8-0.3

Change From Baseline in Pain Characteristics and Intensity as Assessed by the Short Form-McGill Pain Questionnaire (SF-MPQ) at EOMT Using LOCF Data

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)

,,,,
Interventionscores on a scale (Least Squares Mean)
SF-MPQ Total ScoreSF-MPQ Sensory ScoreSF-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

Change From Baseline in Pain Quality as Assessed by the Neuropathic Pain Scale (NPS) Summary Scores at EOMT Using LOCF Data

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)

,,,,
Interventionscores on a scale (Least Squares Mean)
NPS 10 ScoreNPS 8 ScoreNPS Non-Allodynic ScoreNPS 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

Change From Baseline in Quality of Life as Assessed by the 36-Item Short Form Health Survey (SF-36) at EOMT Using LOCF Data

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)

,,,,
Interventionscores on a scale (Least Squares Mean)
SF-36 Physical Component Summary ScoreSF-36 Mental Component Summary Score
GEn 1200 mg/Day3.50.4
GEn 2400 mg/Day3.71.5
GEn 3600 mg/Day4.61.6
PGB 300 mg/Day3.70.7
Placebo3.12.5

Change From Baseline in Severity of Pain and the Impact of Pain as Assessed by the Brief Pain Inventory (BPI) at EOMT Using LOCF Data

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

,,,,
Interventionscores on a scale (Least Squares Mean)
Brief Pain Inventory Severity of PainBrief 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

Number of Participants Achieving Various Levels of Percent Reduction From Baseline in the Mean 24-hour Average Pain Intensity Score at EOMT Using LOCF Data

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)

,,,,
Interventionparticipants (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 baseline100% reduction from baseline
GEn 1200 mg/Day55433631282621171154
GEn 2400 mg/Day504234251915116521
GEn 3600 mg/Day101917866554641251785
PGB 300 mg/Day55423628201495433
Placebo103867357463526151143

Reviews

3 reviews available for carbamates and Nerve Pain

ArticleYear
ADMET considerations for restless leg syndrome drug treatments.
    Expert opinion on drug metabolism & toxicology, 2012, Volume: 8, Issue:10

    Topics: Amines; Anticonvulsants; Benzothiazoles; Carbamates; Cyclohexanecarboxylic Acids; Dopamine Agents; D

2012
Modulation of neuropathic-pain-related behaviour by the spinal endocannabinoid/endovanilloid system.
    Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2012, Dec-05, Volume: 367, Issue:1607

    Topics: Amides; Amidohydrolases; Animals; Arachidonic Acid; Arachidonic Acids; Behavior; Benzamides; Carbama

2012
Inhibition of fatty acid amide hydrolase: a potential treatment for neuropathic pain.
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007, Mar-28, Volume: 27, Issue:13

    Topics: Amidohydrolases; Animals; Benzamides; Carbamates; Mice; Neuralgia; Rats

2007

Trials

1 trial available for carbamates and Nerve Pain

ArticleYear
A randomized, controlled trial of gabapentin enacarbil in subjects with neuropathic pain associated with diabetic peripheral neuropathy.
    Pain practice : the official journal of World Institute of Pain, 2013, Volume: 13, Issue:6

    Topics: Adult; Aged; Aged, 80 and over; Carbamates; Diabetic Neuropathies; Dose-Response Relationship, Drug;

2013

Other Studies

19 other studies available for carbamates and Nerve Pain

ArticleYear
FSC231 alleviates paclitaxel-induced neuralgia by inhibiting the interactions between PICK1 and GluA2 and activates GSK-3β and ERK1/2.
    Brain and behavior, 2021, Volume: 11, Issue:11

    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.
    Neuroscience letters, 2021, 01-10, Volume: 741

    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.
    Brain research bulletin, 2021, Volume: 175

    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.
    Journal of neuroinflammation, 2018, Jan-08, Volume: 15, Issue:1

    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.
    Anesthesia and analgesia, 2019, Volume: 129, Issue:2

    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.
    The Journal of pharmacology and experimental therapeutics, 2018, Volume: 367, Issue:3

    Topics: Amidohydrolases; Analgesics, Opioid; Animals; Antineoplastic Agents; Arachidonic Acids; Benzamides;

2018
Activation of KCNQ Channels Prevents Paclitaxel-Induced Peripheral Neuropathy and Associated Neuropathic Pain.
    The journal of pain, 2019, Volume: 20, Issue:5

    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
    Pharmacological research, 2019, Volume: 142

    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.
    PloS one, 2013, Volume: 8, Issue:4

    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.
    PloS one, 2014, Volume: 9, Issue:5

    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.
    Cellular and molecular neurobiology, 2015, Volume: 35, Issue:1

    Topics: Animals; Carbamates; Ligation; Male; Neuralgia; Neuroprotective Agents; Nitric Oxide; Pain Threshold

2015
Selective monoacylglycerol lipase inhibitors: antinociceptive versus cannabimimetic effects in mice.
    The Journal of pharmacology and experimental therapeutics, 2015, Volume: 353, Issue:2

    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.
    British journal of pharmacology, 2016, Volume: 173, Issue:1

    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.
    The Journal of pharmacology and experimental therapeutics, 2016, Volume: 357, Issue:1

    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.
    European journal of pain (London, England), 2016, Volume: 20, Issue:8

    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.
    Neuropharmacology, 2017, 03-01, Volume: 114

    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.
    European journal of pharmacology, 2003, Jan-24, Volume: 460, Issue:2-3

    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.
    British journal of pharmacology, 2006, Volume: 147, Issue:3

    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].
    Anales espanoles de odontoestomatologia, 1974, Volume: 33, Issue:3

    Topics: Carbamates; Diazepam; Glossopharyngeal Nerve; Humans; Neuralgia

1974