2. Membrane Transporter/Ion Channel Neuronal Signaling
  3. GABA Receptor Sodium Channel iGluR
  4. BTS 72664

BTS 72664 是一种广谱、非镇静性、口服有效的抗惊厥剂，其抗惊厥作用主要源于增强 GABAA 受体 (GABAA receptor) 介导的氯通道电流，同时对 Na⁺ 通道 (Ki = 350 μM) 和 NMDA 受体 (NMDA receptor) (IC50 = 43 μM) 有弱阻断作用。BTS 72664 可阻止神经元外谷氨酸、甘氨酸和丝氨酸浓度升高，减小脑梗死面积，促进功能恢复，预防多种类型癫痫发作，且镇静潜能较低。BTS 72664 可用于癫痫、脑卒中及偏头痛的研究。

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BTS 72664

BTS 72664 Chemical Structure

CAS No. : 165383-52-8

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BTS 72664 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

BTS 72664 is a broad-spectrum, non-sedating, orally effective anticonvulsant. Its anticonvulsant effect mainly arises from enhancing GABAA receptor (GABAA receptor)-mediated chloride channel currents, while it exerts weak blocking effects on Na+ channels (Ki = 350 μM) and NMDA receptors (NMDA receptor) (IC50 = 43 μM). BTS 72664 prevents the elevation of extracellular glutamate, glycine and serine concentrations in neurons, reduces cerebral infarct size, promotes functional recovery, prevents multiple types of epileptic seizures, and has low sedative potential. BTS 72664 can be used for the research of epilepsy, stroke and migraine[1].

体外研究
(In Vitro)

BTS 72664 (350 μM) 可弱结合于大鼠脑突触体膜中的电压门控 Na+通道，其 Ki 值为 350 μM[1]。
BTS 72664 (300 μM; 0-6 seconds) 可使经去极化、Ca2+ 处理的大鼠脑突触体的 86Rb+ 外流显著降低 50%[1]。
BTS 72664 可抑制 Veratridine (HY-N6691) 诱导的大鼠脑突触体谷氨酸外流，且不改变基础外流[1]。
BTS 72664 (3-100 μM) 在大鼠大脑皮质脑片中可使 NMDA 诱导的去极化作用微弱降低约 20%，对非 NMDA 谷氨酸受体无显著活性[1]。
BTS 72664 (0.3-300 μM) 可减弱大鼠脑皮质脑片的自发性癫痫样放电，其对 Bicuculline (HY-N0219) 诱导的 SED 的效力 (频率 IC50 为 94 μM) 强于对去除 Mg2+诱导的 SED 的效力 (频率 IC50 为 189 μM)[1]。
BTS 72664 (100 μM; 20-45 min) 可使大鼠海马脑片 CA1 锥体神经元的静息膜电位超极化，平均超极化幅度为 9.5 mV[1]。
BTS 72664 (10-100 μM) 可减弱培养的瑞士小鼠皮质神经元中 NMDA 诱发的电流，其 IC50 为 43 μM[1]。
BTS 72664 (10-100 μM) 可通过不依赖苯二氮䓬、对 Picrotoxin (HY-101391) 敏感的 GABAA 通道机制增强培养的瑞士小鼠皮质神经元中 GABA 诱发的电流，在 100 μM 时可产生 511% 的增强作用[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

BTS 72664 相关抗体:
体内研究
(In Vivo)

BTS 72664 (1.9-9.4 mg/kg；口服；单次给药；每日一次；连续 5 天) 可强效保护小鼠对抗 Bicuculline 诱导的癫痫发作，其峰值效应下的口服 ED50 为 1.9 mg/kg，且连续 5 天每日给药未出现快速耐受现象[1]。
BTS 72664 (47.5-77.2 mg/kg；口服；单次给药) 可预防小鼠中最大电休克诱导的癫痫发作，其口服给药达峰效应时的 ED50 为 47.5 mg/kg，作用时长为 4-6 hours，且在提高癫痫发作阈值方面的效力强于阻断癫痫发作泛化[1]。
BTS 72664 (14 mg/kg；口服；单剂量) 可预防戊四氮诱导的小鼠癫痫发作，其口服 ED50 为 14 mg/kg，且在提高癫痫发作起始阈值方面具有极高的活性[1]。
BTS 72664 (60 mg/kg；口服；单次给药) 可保护小鼠免受 Picrotoxin 诱导的癫痫发作，其口服 ED50 为 60 mg/kg[1]。
BTS 72664 (25 mg/kg；口服；单次给药) 可预防小鼠由 4-aminopyridine (HY-B0604) 诱导的癫痫发作，其口服 ED50 为 25 mg/kg[1]。
BTS 72664 (18 mg/kg；口服；单次给药) 可预防小鼠由 NMDA (HY-17551) 诱导的癫痫发作，其口服 ED50 为 18 mg/kg[1]。
BTS 72664 (9 mg/kg；口服；单次给药) 可对 DBA/2 小鼠的听源性癫痫发作起到保护作用，其口服 ED50 为 9 mg/kg[1]。
BTS 72664 (29 mg/kg；口服；单次给药) 可对 GEPR-9 大鼠的癫痫发作起到保护作用，其口服 ED50 为 29 mg/kg[1]。
BTS 72664 (4.6 mg/kg；口服；单次给药) 可预防 Bicuculline 诱导的大鼠癫痫发作，其口服 ED50 为 4.6 mg/kg，与小鼠相比效力的种属差异极小[1]。
BTS 72664 (90 mg/kg；口服；单次给药) 可预防大鼠中最大电休克诱导的癫痫发作，其口服 ED50 为 90 mg/kg，与小鼠相比效力的物种差异极小[1]。
BTS 72664 (100-150 mg/kg；口服；单次给药) 可剂量依赖性地改善杏仁核点燃大鼠的癫痫发作参数，其中 150 mg/kg 口服剂量可使癫痫发作阈值升高 177%，癫痫发作持续时间缩短 65%[1]。
BTS 72664 (50 mg/kg；口服；每 12 小时 1 次；共给药 4 次)，可使永久性大脑中动脉闭塞的褐家鼠的缺血性病灶体积减少 31%，并促进其功能恢复[1]1]。
BTS 72664 (20-35 mg/kg；腹腔注射；初始单次给药；每 12 小时 1 次；后续给药 3 次)，于栓塞后 60 分钟开始给药，可使永久性大脑中动脉栓塞大鼠的缺血病灶体积减少 40%，且该神经保护作用无低温因素参与[1]。
BTS 72664 (50 mg/kg；口服；单次给药)，于大鼠皮层损伤后 15 分钟给药，可快速且持续地消除皮层扩散性抑制相关的大鼠细胞外谷氨酸、甘氨酸和丝氨酸水平升高[1]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Swiss CD1 mice[1]
Dosage: 1.9 mg/kg (30 min post-dose); 9.4 mg/kg (60 min post-dose); 2.8 mg/kg (chronic)
Administration: p.o.; single dose; p.o.; daily; 5 days
Result: Had an ED50 of 1.9 mg/kg p.o.
for protection against bicuculline-induced seizures at 30 min post-dose.
Had an ED50 of 9.4 mg/kg p.o.
for protection against bicuculline-induced seizures at 60 min post-dose.
Showed no significant attenuation of anticonvulsant efficacy after 5 consecutive days of 2.8 mg/kg p.o.
daily dosing compared to a single dose.
Animal Model: Swiss CD1 mice[1]
Dosage: 47.5 mg/kg (30 min post-dose); 77 mg/kg (60 min post-dose); 77.2 mg/kg (peak protection)
Administration: p.o.; single dose
Result: Had an ED50 of 47.5 mg/kg p.o.
for protection against maximal electroshock-induced seizures at 30 min post-dose.
Had an ED50 of 77 mg/kg p.o.
for protection against maximal electroshock-induced seizures at 60 min post-dose.
Provided peak protection against maximal electroshock-induced seizures at 30 min post-dose with a duration of action of 4-6 hours at 77.2 mg/kg p.o.
Had a TID20 of 5.7 mg/kg p.o.
for increasing seizure current threshold by 20%.
Animal Model: Swiss CD1 mice[1]
Dosage: 14 mg/kg
Administration: p.o.; single dose
Result: Had an ED50 of 14 mg/kg p.o.
for protection against subcutaneous pentylenetetrazol-induced seizures.
Had a TID20 of 5.6 mg/kg p.o.
for increasing pentylenetetrazol-induced initial myoclonic twitch threshold by 20%.
Had a TID20 of 1.1 mg/kg p.o.
for increasing pentylenetetrazol-induced generalized clonic seizure threshold by 20%.
Animal Model: Swiss CD1 mice[1]
Dosage: 60 mg/kg
Administration: p.o.; single dose
Result: Had an ED50 of 60 mg/kg p.o.
for protection against subcutaneous picrotoxin-induced seizures.
Animal Model: Swiss CD1 mice[1]
Dosage: 25 mg/kg
Administration: p.o.; single dose
Result: Had an ED50 of 25 mg/kg p.o.
for protection against intracerebroventricular 4-aminopyridine-induced seizures.
Animal Model: Swiss CD1 mice[1]
Dosage: 18 mg/kg
Administration: p.o.; single dose
Result: Had an ED50 of 18 mg/kg p.o.
for protection against intracerebroventricular NMDA-induced seizures.
Animal Model: DBA/2 mice[1]
Dosage: 9 mg/kg
Administration: p.o.; single dose
Result: Had an ED50 of 9 mg/kg p.o.
for protection against audiogenic seizures in DBA/2 mice.
Animal Model: GEPR-9 rats[1]
Dosage: 29 mg/kg
Administration: p.o.; single dose
Result: Had an ED50 of 29 mg/kg p.o.
for protection against seizures in GEPR-9 rats.
Animal Model: Rats[1]
Dosage: 4.6 mg/kg
Administration: p.o.; single dose
Result: Had an ED50 of 4.6 mg/kg p.o.
for protection against bicuculline-induced seizures in rats.
Animal Model: Rats[1]
Dosage: 90 mg/kg
Administration: p.o.; single dose
Result: Had an ED50 of 90 mg/kg p.o.
for protection against maximal electroshock-induced seizures in rats.
Animal Model: Rats[1]
Dosage: 100 mg/kg; 150 mg/kg
Administration: p.o.; single dose
Result: Increased mean kindled seizure threshold by 68% at 100 mg/kg p.o.
Increased mean kindled seizure threshold by 177% at 150 mg/kg p.o.
Reduced mean seizure severity by 59% at 150 mg/kg p.o.
Reduced mean seizure duration by 65% (from 69 to 24 sec) at 150 mg/kg p.o.
Reduced mean afterdischarge duration by 68% (from 105 to 34 sec) at 150 mg/kg p.o.
Caused mild ataxia at 150 mg/kg p.o.
but no significant motor impairment in the rotarod test.
Animal Model: Rats[1]
Dosage: 50 mg/kg
Administration: p.o.; every 12 hours; 4 total doses
Result: Reduced cerebral lesion volume by 31% (treated: 56.9 mm3; vehicle: 82.6 mm3) at 2 days post-insult.
Showed a significant reduction in contralateral forelimb faults on day 8 post-insult, and when data from days 3, 6, and 8 were combined, compared to vehicle-treated controls.
Animal Model: Rats[1]
Dosage: 20 mg/kg (subsequent doses); 35 mg/kg (initial dose)
Administration: i.p.; single initial dose; i.p.; every 12 hours; 3 subsequent doses
Result: Reduced cerebral lesion volume by 40% (treated: 43.6 mm3; vehicle: 72.0 mm3) at 6 days post-insult.
Did not decrease core body temperature when monitored for 18 hours after the initial 35 mg/kg i.p.
dose.
Animal Model: Rats[1]
Dosage: 50 mg/kg
Administration: p.o.; single dose
Result: Abolished the transient, insult-induced increases in extracellular glutamate, glycine, and serine levels in the parietal cortex.
Did not alter extracellular GABA levels, but reduced extracellular glutamate levels compared to basal values in anesthetic-only controls.
Exhibited a rapid onset (30 min post-administration) and effect lasting for at least 2.25 hours from peak brain levels.
分子量

274.71

Formula

C13H11ClN4O
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

BTS 72664 相关分类

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Keywords:

BTS 72664165383-52-8BTS72664BTS-72664GABA ReceptorSodium ChanneliGluRGamma-aminobutyric acid Receptorγ-Aminobutyric acid ReceptorNa channelsNa+ channelsIonotropic glutamate receptorsNMDA channelrat brain synaptosomal membranessodium channelmigraineSwiss mouse cortical neuronschloride channelepilepsystrokerat hippocampal slice CA1 pyramidal neuronshuman lymphocyteInhibitorinhibitorinhibit

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