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

α,β-Methylene-ATP dilithium is an agonist of P2X1 and P2X3 receptors and can cross the blood-brain barrier. α,β-Methylene-ATP dilithium 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 dilithium 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 dilithium can be used to study the pathological mechanisms of neuropathic pain, cardiovascular reflex regulation, and antinociceptive effects of the central nervous system.

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α,β-Methylene-ATP dilithium Chemical Structure

α,β-Methylene-ATP dilithium Chemical Structure

CAS No. : 104809-20-3

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Based on 1 publication(s) in Google Scholar

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Description

α,β-Methylene-ATP dilithium is an agonist of P2X1 and P2X3 receptors and can cross the blood-brain barrier. α,β-Methylene-ATP dilithium 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 dilithium 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 dilithium 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].

IC50 & Target

p2x1 Receptor

 

P2X3 Receptor

 

P2X7 Receptor

 

In Vitro

Electrophysiological activity: α,β-Methylene-ATP trisodium (10 μM; 3 seconds) evokes a fast inward current in rat dorsal root ganglion (DRG) neurons, associated with P2X3 receptor activation. 10 μM Diinosine pentaphosphate (Ip5I) can significantly inhibit this inward current[1].
α,β-Methylene-ATP trisodium (10 μM; transient) enhances the amplitude of the current evoked by Acetylcholine (HY-B0282) in rat adrenal medullary chromaffin cells and increases the proportion of the current sensitive to α-conotoxin RgIA (HY-P5845)[1].

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

In Vivo

α,β-Methylene-ATP (5-50 μg/kg; left popliteal artery injection; single dose) dilithium induces a reflex pressor response in the decerebrate cat model, which is blocked by sciatic nerve transection or the P2X receptor antagonist PPADS (HY-108960) (10 mg/kg; left popliteal artery injection)[2].
α,β-Methylene-ATP (10 nmol/rat; intracerebroventricular injection; single dose) dilithium produces an anti-mechanical nociceptive effect in Sprague-Dawley rats, which is significantly attenuated by pretreatment with DSP-4 (HY-121602/HY-103210) (10 mg/kg DSP-4; intraperitoneal injection)[3].
α,β-Methylene-ATP (0.1-1 nmol/side; bilateral microinjection into the locus coeruleus; single dose) dilithium increases the pain threshold of Sprague-Dawley rats in a dose-dependent manner, an effect that could be antagonized by co-injection of PPADS (HY-108960) (0.1-1 nmol/side)[3].

MedChemExpress (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 α,β-Methylene-ATP
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.
Molecular Weight

519.09

Formula

C11H18Li2N5O12P3

CAS No.
SMILES

OP(OP(CP(OC[C@@H]1[C@@H](O)[C@@H](O)[C@H](N2C3=NC=NC(N)=C3N=C2)O1)(O)=O)(O)=O)(O)=O.[Li].[Li]

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Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
References
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Product Name:
α,β-Methylene-ATP dilithium
Cat. No.:
HY-134440
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