2. Membrane Transporter/Ion Channel
  3. P2X Receptor
  4. α,β-Methylene-ATP

α,β-Methylene-ATP 是 P2X1 和 P2X3 受体的激动剂，能够透过血脑屏障。α,β-Methylene-ATP 可通过激活外周肌肉和中枢蓝斑核 (LC) 的 P2X 受体，引发反射性升压反应；该效应可被 P2X 拮抗剂 PPADS (HY-108960) 阻断。α,β-Methylene-ATP 还激活中枢蓝斑核的去甲肾上腺素能神经元，介导抗伤害作用；该效应可被蓝斑核损伤剂 DSP-4 (HY-103210/HY-121602) 削弱。α,β-Methylene-ATP 可用于研究神经性疼痛病理机制、心血管反射调节及中枢神经系统的抗伤害作用。

该游离形式化合物不稳定，推荐具有相同生物学活性的稳定盐形式 α,β-Methylene-ATP trisodium。

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α,β-Methylene-ATP Chemical Structure

α,β-Methylene-ATP Chemical Structure

CAS No. : 7292-42-4

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α,β-Methylene-ATP 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

α,β-Methylene-ATP is an agonist of P2X1 and P2X3 receptors and can cross the blood-brain barrier. α,β-Methylene-ATP can trigger a reflex pressor response by activating P2X receptors in peripheral muscles and the central locus coeruleus (LC); this effect can be blocked by the P2X antagonist PPADS (HY-108960). α,β-Methylene-ATP also activates noradrenergic neurons in the central locus coeruleus, mediating antinociceptive effects; this effect can be attenuated by the locus coeruleus damaging agent DSP-4 (HY-103210/HY-121602). α,β-Methylene-ATP can be used to study the pathological mechanisms of neuropathic pain, cardiovascular reflex regulation, and antinociceptive effects of the central nervous system[1][2][3].

体外研究
(In Vitro)

电生理活性：
α,β-Methylene-ATP (10 μM；3 秒) 在大鼠背根神经节 (DRG) 神经元中诱发快速内向电流，与 P2X3 受体激活有关。10 μM Diinosine pentaphosphate (Ip5I) 可显著抑制这种内向电[1]。
α,β-Methylene-ATP (10 μM；瞬时) 在大鼠肾上腺髓质嗜铬细胞 (Chromaffin cells) 中增强 Acetylcholine (HY-B0282) 诱发的电流幅度，且对 α-conotoxin RgIA (HY-P5845) 敏感的电流比例增加[1]。

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

α,β-Methylene-ATP 相关抗体:
体内研究
(In Vivo)

α,β-Methylene-ATP (5-50 μg/kg；左侧腘动脉注射；单剂量) 在去大脑猫模型中诱发反射性升压反应，该反应可被坐骨神经切断或 P2X 受体拮抗剂 PPADS (HY-108960) (10 mg/kg；左腘动脉注射) 阻断[2]。
α,β-Methylene-ATP (10 nmol/rat；脑室内注射；单剂量) 在 Sprague-Dawley 大鼠中产生抗机械伤害作用，该作用可被 DSP-4 (HY-121602/HY-103210) (10 mg/kg DSP-4；腹腔注射) 预处理显著减弱[3]。
α,β-Methylene-ATP (0.1-1 nmol/side；双侧蓝斑核微注射；单剂量) 在 Sprague-Dawley 大鼠中，以剂量依赖性升高大鼠的疼痛阈值，该效应可被 PPADS (HY-108960) (0.1-1 nmol/side) 共注射拮抗[3]。

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

Animal Model: Decerebrate cats[2]
Dosage: 5, 20, 50 µg/kg
Administration: Left popliteal artery injection, single dose
Result: Significantly increased mean arterial pressure.
The pressor response was attenuated by sciatic nerve section and completely blocked by prior popliteal artery injection of PPADS (10 mg/kg), indicating involvement of P2X receptors in muscle afferents.
Animal Model: Sprague-Dawley rats (male, 180-250 g, 6-8 weeks old)[3]
Dosage: 10 nmol/rat
Administration: Intracerebroventricular injection, single dose
Result: Elevated the mechanical nociceptive threshold by 63.6% at 5 min post-injection. Pretreatment with DSP-4 (50 mg/kg, i.p.), a noradrenergic neurotoxin, reduced the antinociceptive effect to baseline levels, suggesting involvement of locus coeruleus noradrenergic neurons.
Animal Model: Sprague-Dawley rats (male, 180-250 g, 6-8 weeks old)[3]
Dosage: 0.1-1 nmol/side
Administration: Bilateral locus coeruleus microinjection, single dose, no cycle
Result: Dose-dependently increased the nociceptive threshold (peak at 5 min, 117.9% above control at 1 nmol/side).
Co-injection of PPADS (1 nmol/side) completely antagonized the antinociceptive effect, confirming P2X receptor-mediated mechanism.
分子量

505.21

Formula

C11H18N5O12P3
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

α,β-Methylene-ATP 相关分类

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Keywords:

α,β-Methylene-ATP7292-42-4P2X ReceptorP2XRsInhibitorinhibitorinhibit

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