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pregabalin (pregabalin, YuHan / YHD 1119 / YHD1119)

✓ Approved

YuHan · CACNA2D1 · 小分子

什么是 pregabalin？

pregabalin 是一种小分子，由YuHan研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名pregabalin, YuHan, YHD 1119, YHD1119
公司YuHan
药物类别小分子
分子靶点CACNA2D1
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, YuHan

作用机制

分子靶点

pregabalin 作用于 1 个分子靶点：

CACNA2D1calcium voltage-gated channel auxiliary subunit alpha2delta 1 (LINC01112, CACNA2)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

pregabalin 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Nervous system disordersDiabetic neuropathy✓ Approved
Nervous system disordersPost herpetic neuralgia✓ Approved

相关研究文献

PubMedJournal of pain research2026-06-12

Effect of Erector Spinae Plane Block Applied to Painful Herpes Zoster Patients Who Failed to Respond to Pregabalin Treatment on Immunological Marker Levels and Postherpetic Neuralgia Incidence Rate.

Büyükbezirci Gülçin G, Demiralp Numan N, Keles Sevgi S, Yılmaz Resul R et al.

Postherpetic neuralgia (PHN) is one of the most debilitating complications of herpes zoster and represents a major cause of chronic neuropathic pain. Increasing evidence suggests that immune dysregulation plays a critical role in neuropathic pain development. This study aimed to investigate the effects of the erector spinae plane (ESP) block on PHN development and immunological marker levels in herpes zoster patients who did not respond to pregabalin therapy. This prospective, controlled, single‑blind, non-randomized study included 30 patients with herpes zoster. Pregabalin therapy was initiated in all patients. Patients whose pain was adequately controlled with pregabalin were assigned to Group I, whereas patients with insufficient pain control received an ESP block and were assigned to Group II. Blood samples were collected at baseline, after treatment response, and at the three-month follow-up. T‑cell subsets and natural killer (NK) cell subgroups were analyzed using flow cytometry. Pain intensity, sleep interference, and PHN incidence were evaluated during follow-up. Pain and sleep interference scores improved significantly over time in both groups (P < 0.05).The incidence of PHN did not differ significantly between the groups. However, at the three-month follow-up, patients in the ESP block group, who were receiving higher pregabalin doses, demonstrated lower CD3⁺ and CD4⁺ T-cell levels and reduced NK cell subset levels compared with Group I (P < 0.05).Baseline NK CD56 Bright levels were significantly higher in patients who did not develop PHN (P < 0.05). Although the ESP block did not reduce the incidence of PHN, immunological differences were observed between the treatment groups during follow-up. Higher baseline NK CD56 Bright levels in patients who did not develop PHN suggest a potential protective association between preserved NK-cell-mediated immunity and resistance to pain chronification following herpes zoster.

PMID 42281611
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PubMedInternational journal of molecular sciences2026-06-12

Pregabalin Depresses Cerebellar Parallel Fiber-Purkinje Cell Synaptic Transmission by Modulating Glun2a-Containing Nmda Receptors in Mice In Vitro.

Li Mei-Rui MR, Zhang Xu-Dong XD, Chen Li L, Zhang Yi-Dan YD et al.

Pregabalin (PGB) exerts its therapeutic effects by binding to the α2δ auxiliary subunits of voltage-gated calcium channels and modulates synaptic transmission in the brain. However, its influence on cerebellar parallel fiber-Purkinje cell (PF-PC) synaptic transmission remains unclear. In the present study, we investigated the effects of PGB on PF-PC synaptic transmission using whole-cell patch-clamp recording, glutamate fluorescence imaging, immunohistochemistry, co-immunoprecipitation, Western blotting, and pharmacological approaches. Micro-application of PGB to the cerebellar molecular layer induced a concentration-dependent inhibition of PF-PC excitatory postsynaptic currents (EPSCs), accompanied by an increased paired-pulse ratio. The inhibitory effect of PGB on PF-PC EPSCs was abolished by extracellular blockade of N-methyl-D-aspartate receptors (NMDAR) or their GluN2A subtype, as well as by disruption of α2δ-1-NMDAR complexes, but not by intracellular NMDAR inhibition. Glutamate sensor imaging further showed that PGB markedly reduced the fluorescence intensity of glutamate release evoked by PF stimulation. In the presence of tetrodotoxin (TTX) and a gamma-aminobutyric acid type A (GABAA) receptor antagonist, PGB reduced the frequency of miniature excitatory postsynaptic currents (mEPSCs) without affecting their amplitude. The PGB-induced reduction in mEPSC frequency was fully abolished by extracellular blockade of GluN2A-containing NMDARs or disruption of α2δ-1-NMDAR complexes. Similarly, the inhibitory effects of PGB on PF-PC EPSCs and mEPSCs were eliminated by extracellular PKA inhibition, but not by intracellular protein kinase A (PKA) inhibition. Western blot analysis showed that PGB significantly increased PKA phosphorylation in the molecular layer of the cerebellar cortex. Immunoreactivity for GluN2A and α2δ-1 subunits was colocalized within the molecular layer and abundantly distributed around the dendrites and somata of PCs. Co-immunoprecipitation further verified that α2δ-1 was co-precipitated with GluN1 in cerebellar molecular layer tissue samples. The results indicate that PGB depresses glutamate release from parallel-fiber terminals in the mouse cerebellar cortex through the presynaptic α2δ-1-coupled GluN2A-containing NMDAR/PKA signaling pathway, thereby attenuating PF-PC synaptic transmission.

PMID 42278194
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PubMedPhytomedicine : international journal of phytotherapy and phytopharmacology2026-06-12

Angelica dahurica alleviates peripheral nerve injury-induced muscle atrophy via the Phlpp2-Akt-FoxO3α axis independently of analgesia.

Wu Dan D, Wang Ping P, Liu Xin X, Li Han H et al.

Peripheral nerve injury frequently causes refractory neuropathic pain and muscle atrophy. While clinical care focuses on analgesia, effective therapies for muscle wasting are lacking. Angelica dahurica (BZ) is known for its analgesic properties, but whether it also ameliorates muscle atrophy remains unclear. This study evaluates the dual analgesic and anti‑atrophic effects of BZ, with a focus on determining whether its muscle‑protective action is separable from pain relief and elucidating the underlying mechanism. Following sciatic nerve chronic constriction injury (CCI), rats were treated with BZ extract or Pregabalin (Pre), a positive analgesic control. Nociceptive behaviors and motor function were assessed via behavioral tests and gait analysis. Muscle atrophy was evaluated by wet weight, histology, and transmission electron microscopy. RNA‑seq was performed to profile transcriptomic changes in muscle. High‑resolution mass spectrometry was used to identify BZ‑derived components in plasma and muscle. Post-CCI muscle atrophy and pain showed distinct temporal trajectories, with atrophy transitioning from an acute phase of rapid mass loss (days 1-10) to a later phase of progressive fibrosis (days 14-21). BZ administration significantly alleviated mechanical, cold, and thermal hypersensitivity, while concurrently increasing muscle mass and partially improving myofiber morphology and sarcomere ultrastructure. Notably, while Pre provided equivalent analgesia, it failed to mitigate muscle atrophy, demonstrating that the anti-atrophic effect of BZ is largely independent of its analgesic activity. Mechanistically, BZ-mediated recovery was associated with the modulation of the intramuscular Phlpp2‑Akt‑ FoxO3α signaling axis, as indicated by suppressed Phlpp2 expression and enhanced Akt phosphorylation. Seven muscle-distributed components were identified as potential contributors to these therapeutic effects. BZ exerts potential anti-atrophic effects that correlated with modulation of the Phlpp2‑Akt‑FoxO3α axis, largely independent of its analgesic activity. These findings identify BZ as a promising dual-action therapeutic candidate for addressing both neuropathic pain and muscle wasting following peripheral nerve injury.

PMID 42275876
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PubMedBMC anesthesiology2026-06-10

The effect of pregabalin for pain after third molar surgery: a systematic review and meta-analysis.

Li Jie J, Wang Anli A

Pregabalin has been proposed as an adjunct for postoperative pain management following third molar surgery, but its analgesic efficacy, safety, and clinical applicability remain uncertain. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) ascertaining pregabalin for pain after third molar extraction. A systematic search was conducted across PubMed, Scopus, Web of Science, and Google Scholar up to January 2025. RCTs appraising pregabalin for postoperative pain following third molar surgery were included. The primary outcome was pain intensity (VAS) and the secondary outcome was adverse events (AEs). Data were pooled using a random-effects meta-analysis, with mean difference (MD) for pain scores and odds ratio (OR) for AEs, each with 95% confidence intervals (CIs). Risk of bias was assessed using the Cochrane RoB 2 tool. Six RCTs involving 545 patients undergoing third molar surgery were included. Of these, 170 patients (4 RCTs) contributed data to the quantitative synthesis. Pregabalin significantly mitigated postoperative pain compared with control (MD - 0.99, 95% CI - 1.46 to - 0.52, p < 0.00001), though substantial heterogeneity was observed (I²=91%). Subgroup analysis by timepoint revealed consistent but individually nonsignificant reductions in pain at 2-24 h postoperatively. Pregabalin use was linked to a higher risk of adverse events (OR 4.36, 95% CI 2.52-7.55, p < 0.00001, I²=77%), with a dose-response effect observed (ORs: 1.18 for 50 mg, 5.19 for 75 mg, 11.16 for 300 mg). Risk of bias was high or raised some concerns in three of the six included trials, with the certainty of evidence being limited by the substantial heterogeneity. Pregabalin may provide a modest reduction in postoperative pain following third molar surgery; however, the clinical relevance and robustness of this benefit remain uncertain due to substantial heterogeneity and sensitivity to a single study. In contrast, pregabalin was consistently associated with an increased risk of adverse events. Therefore, the benefit-harm balance does not clearly support routine use of pregabalin as a first-line analgesic in this setting. Further high-quality, placebo-controlled RCTs with standardized dosing, comparator groups, and postoperative assessment timepoints are needed.

PMID 42265625
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PubMedCureus2026-06-10

Cervical Myelopathy Associated With Deep Neck Muscle Rhabdomyolysis After Polysubstance Abuse: A Case Report.

Pfannenbecker Sofia C SC, Prabu Mohan M, Wei Olivia O, Javan Ramin R

Rhabdomyolysis is a potentially life-threatening syndrome caused by skeletal muscle breakdown and the release of intracellular contents into circulation, often resulting in complications such as acute kidney injury. Although it most commonly affects the limbs, rhabdomyolysis of the deep neck muscles is rare and can lead to secondary cervical myelopathy. Recent reports have highlighted a strong association with polysubstance abuse, particularly combinations of opioids with sedatives such as benzodiazepines or pregabalin. We describe a 41-year-old female patient who developed acute quadriparesis following polysubstance use involving pregabalin, methamphetamine, buprenorphine, and alcohol. MRI revealed a longitudinal T2-hyperintense cervical cord lesion from C2 to T3 with marked paravertebral muscle edema, consistent with deep neck muscle rhabdomyolysis. Laboratory findings showed a creatine phosphokinase peak of 16,093 U/L, which normalized with corticosteroid therapy and intravenous hydration. Despite normalization of laboratory values, the patient had persistent limb weakness at discharge due to venous hypertensive myelopathy, inadvertently caused by deep cervical rhabdomyolysis. This case reinforces emerging evidence that deep cervical muscle rhabdomyolysis can lead to venous hypertensive myelopathy through a compartment-syndrome-like mechanism. Awareness of this presentation is essential, as early MRI of both the spinal cord and paravertebral musculature may enable timely diagnosis and improved outcomes in polysubstance-related myelopathy.

PMID 42266304
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PubMedPain medicine case reports2026-06-09

Spinal Cord Stimulation and Improved Hand Function in a Traumatic Upper Limb Replantation: A Case Report.

Fisher Mitchell M, Nagesh Dhruv D, Gupta Mayank M

Spinal cord stimulation (SCS) is commonly used to treat chronic pain that is refractory to conservative management. SCS has demonstrated efficacy in reducing paresthesia and pain, but functional motor improvements after this type of intervention are reported less often. A 70-year-old man sustained a traumatic left forearm amputation in 2015, which was followed by surgical reattachment and persistent neuropathic pain. The patient tried several interventions, including nonsteroidal antiinflammatory drugs, muscle relaxants, gabapentin, pregabalin, opioids, duloxetine, and nerve blocks. Ultimately, in 2017, he underwent the implantation of an SCS device. The SCS provided a maximum 90% reduction in pain and eliminated the paresthesias. The pain reduction notably helped double his range of motion when compared to pre-implantation interventions. He demonstrated improved range of motion, reduced muscle atrophy, and increased strength. SCS provided both substantial pain relief and unanticipated functional recovery in this patient, whose upper limb had been amputated. This case serves to highlight a novel therapeutic benefit of SCS beyond pain relief.

PMID 42263292
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