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更新于：2026-08-04
OV-329
更新于：2026-08-04
概要
基本信息
非在研机构- |
权益机构- |
最高研发阶段临床2期 |
首次获批日期- |
最高研发阶段(中国)临床申请批准 |
特殊审评- |
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结构/序列
分子式C7H7F2NO2 |
InChIKeyFBLNZOCTNRXJQD-YFKPBYRVSA-N |
CAS号2093928-28-8 |
关联
4
项与 OV-329 相关的临床试验CTIS2026-527114-23-00
Pharmacodynamic Evaluation of OV329 in Participants with Epilepsy and a Photo-Induced Generalized Epileptiform EEG-Response Phase 2 Proof-of-Concept.
ACTRN12626000488303
A double-blind, placebo-controlled study to evaluate the safety, tolerability and potential antiseizure activity of adjunctive OV-329 in adult focal epilepsy patients.
ACTRN12625001363471
A Follow-on, Ascending, Single and Multiple Dose(s), Double-Blind, Randomized, Placebo Controlled Study Assessing the Safety, Tolerability, and Pharmacokinetics of OV329 in Healthy Male and Female Participants
100 项与 OV-329 相关的临床结果
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100 项与 OV-329 相关的转化医学
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100 项与 OV-329 相关的专利（医药）
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10
项与 OV-329 相关的文献（医药）2025-01-07PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Efficacy of GABA aminotransferase inactivator OV329 in models of neuropathic and inflammatory pain without tolerance or addiction
Article
作者: Xu, Zhili ; Pepin, Robert H. ; Crystal, Jonathon D. ; Wirt, Jonah L. ; Woodward, Taylor J. ; Silverman, Richard B. ; Assis Ferreira, Luana ; Oliva, Idaira ; Hohmann, Andrea G. ; Jesus, Carlos Henrique Alves
Dysregulation of GABAergic inhibition is associated with pathological pain. Consequently, enhancement of GABAergic transmission represents a potential analgesic strategy. However, therapeutic potential of current GABA agonists and modulators is limited by unwanted side effects. We postulated that inhibition of GABA’s degradation enzyme, GABA aminotransferase (GABA-AT), would increase endogenous GABA levels and produce analgesia. We evaluated antinociceptive efficacy of the potent GABA-AT inhibitor OV329 in rodent models of neuropathic and inflammatory pain and assessed possible side effects (i.e., reward and motor impairment). OV329 attenuated the development and maintenance of mechanical and cold hypersensitivities induced by the chemotherapeutic agent paclitaxel. Prophylactic OV329, administered systemically, normalized paclitaxel-induced increases in glutamate levels and suppressed neuropathic nociception. Intrathecal OV329 suppressed paclitaxel-induced mechanical hypersensitivity, elevating GABA, and reducing glutamate levels in the lumbar spinal cord, consistent with a spinal site of action. Furthermore, OV329 largely synergized with paclitaxel to enhance 4T1 tumor cell line cytotoxicity without altering viability of nontumor cells. OV329 also attenuated inflammation-induced mechanical hypersensitivity induced by intraplanar injection of complete Freund’s adjuvant (CFA) with efficacy comparable to morphine. Unlike morphine, OV329 did not produce reward in a conditioned place preference assay in mice and was not self-administered intravenously by rats. Antinociceptive efficacy of OV329 was observed at doses that did not impair motor function or produce tolerance following chronic dosing. Thus, inhibition of GABA-AT with OV329 represents a unique therapeutic strategy to alleviate neuropathic and inflammatory pain with no apparent abuse liability, potentially producing a beneficial spectrum of pharmacological effects through enzymatic regulation.
2024-10-01EPILEPSIA
Progress report on new medications for seizures and epilepsy: A summary of the 17th Eilat Conference on New Antiepileptic Drugs and Devices (EILAT XVII). I. Drugs in preclinical and early clinical development
Article
作者: White, H. Steve ; Johannessen, Svein I. ; Perucca, Emilio ; Tomson, Torbjörn ; Koepp, Matthias J. ; Bialer, Meir ; Perucca, Piero
Abstract:
For >30 years, the Eilat Conference on New Antiepileptic Drugs and Devices has provided a forum for the discussion of advances in the development of new therapies for seizures and epilepsy. The EILAT XVII conference took place in Madrid, Spain, on May 5–8, 2024. Participants included basic scientists and clinical investigators from industry and academia, other health care professionals, and representatives from lay organizations. We summarize in this article information on treatments in preclinical and in early clinical development discussed at the conference. These include AMT‐260, a gene therapy designed to downregulate the expression of Glu2K subunits of kainate receptors, in development for the treatment of drug‐resistant seizures associated with mesial temporal sclerosis; BHV‐7000, a selective activator of heteromeric Kv7.2/7.3 potassium channels, in development for the treatment of focal epilepsy; ETX101, a recombinant adeno‐associated virus serotype 9 designed to increase NaV1.1 channel density in inhibitory γ‐aminobutyric acidergic (GABAergic) neurons, in development for the treatment of SCN1A‐positive Dravet syndrome; GAO‐3‐02, a compound structurally related to synaptamide, which exerts antiseizure activity at least in part through an action on cannabinoid type 2 receptors; LRP‐661, a structural analogue of cannabidiol, in development for the treatment of seizures associated with Lennox–Gastaut syndrome, Dravet syndrome, and tuberous sclerosis complex; OV329, a selective inactivator of GABA aminotransferase, in development for the treatment of drug‐resistant seizures; PRAX‐628, a functionally selective potent sodium channel modulator with preference for the hyperexcitable state of sodium channels, in development for the treatment of focal seizures; RAP‐219, a selective negative allosteric modulator of transmembrane α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor regulatory protein γ‐8, in development for the treatment of focal seizures; and rozanolixizumab, a humanized anti‐neonatal Fc receptor monoclonal antibody, in development for the treatment of LGI1 autoimmune encephalitis. Treatments in more advanced development are summarized in Part II of this report.
2024-07-01eNeuro
Sustained Inhibition of GABA-AT by OV329 Enhances Neuronal Inhibition and Prevents Development of Benzodiazepine Refractory Seizures
Article
作者: Lin, Shinghong ; Davies, Paul A ; Moss, Stephen J ; Mukherjee, Jayanta ; Colmers, Phillip L W ; Arshad, Muhammad Nauman ; Sarmiere, Patrick ; Ng, Shu Fun Josephine
γ-Aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the adult brain which mediates its rapid effects on neuronal excitability via ionotropic GABAAreceptors. GABA levels in the brain are critically dependent upon GABA-aminotransferase (GABA-AT) which promotes its degradation. Vigabatrin, a low-affinity GABA-AT inhibitor, exhibits anticonvulsant efficacy, but its use is limited due to cumulative ocular toxicity. OV329 is a rationally designed, next-generation GABA-AT inhibitor with enhanced potency. We demonstrate that sustained exposure to OV329 in mice reduces GABA-AT activity and subsequently elevates GABA levels in the brain. Parallel increases in the efficacy of GABAergic inhibition were evident, together with elevations in electroencephalographic delta power. Consistent with this, OV329 exposure reduced the severity of status epilepticus and the development of benzodiazepine refractory seizures. Thus, OV329 may be of utility in treating seizure disorders and associated pathologies that result from neuronal hyperexcitability.
100 项与 OV-329 相关的药物交易
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研发状态
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 癫痫 | 临床2期 | 荷兰 | 2026-08-01 | |
| 癫痫发作 | 临床2期 | 美国 | - | |
| 发育性癫痫性脑病 | 临床1期 | 澳大利亚 | - | |
| 婴儿痉挛 | 临床1期 | - | - | |
| 结节性硬化症 | 临床1期 | - | - | |
| 癫痫部分性发作 | 临床申请批准 | 中国 | 2026-07-30 |
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临床结果
临床结果
适应症
分期
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临床1期 | - | 68 | OV329 (1-5 mg) | 鹽願鏇積壓膚製積齋夢(鏇鏇簾範鹹夢窪製繭構) = 蓋鬱選繭顧積壓繭膚醖 壓壓憲糧鏇遞簾膚醖窪 (膚蓋鏇繭積糧鬱齋膚餘 ) 更多 | 积极 | 2025-10-03 | |
Placebo | 鹽願鏇積壓膚製積齋夢(鏇鏇簾範鹹夢窪製繭構) = 繭遞膚憲窪衊簾鬱蓋壓 壓壓憲糧鏇遞簾膚醖窪 (膚蓋鏇繭積糧鬱齋膚餘 ) 更多 |
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