2. Metabolic Enzyme/Protease Neuronal Signaling GPCR/G Protein
  3. Adenosine Kinase Adenosine Receptor
  4. ABT-702 hydrochloride

ABT-702 hydrochloride  (Synonyms: Adenosine Kinase Inhibitor hydrochloride)

目录号: HY-112482A
产品使用指南 技术支持

ABT-702 (hydrochloride) 是一种强效、具有口服活性且选择性的腺苷激酶 (AK) 抑制剂，其 IC50 值为 1.7 nM。ABT-702 (hydrochloride) 对腺苷激酶的选择性比对其他生物靶点 (包括环氧合酶 -1和 -2) 的选择性高出 1300 倍以上。ABT-702 (hydrochloride) 通过提高游离腺苷水平来减轻糖尿病视网膜病变中的炎症。ABT-702 (hydrochloride) 在体内表现出镇痛和抗炎作用。ABT-702 (hydrochloride) 可用于糖尿病视网膜病变的相关研究[1][2][3]。

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ABT-702 hydrochloride

ABT-702 hydrochloride Chemical Structure

CAS No. : 2624336-92-9

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ABT-702 hydrochloride 的其他形式现货产品:

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ABT-702 hydrochloride 相关抗体

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查看 Adenosine Receptor 亚型特异性产品:

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Adenosine A1 receptor (A1R) Adenosine A2A receptor (A2AR) Adenosine A2B receptor (A2BR) Adenosine A3 receptor (A3R)

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

ABT-702 (hydrochloride) is a potent, orally active, and selective adenosine kinase (AK) inhibitor with an IC50 of 1.7 nM. ABT-702 (hydrochloride) shows >1300-fold selectivity for AK over other biological targets, including cyclooxygenases-1 and -2. ABT-702 (hydrochloride) attenuates inflammation in diabetic retinopathy by increasing free adenosine levels. ABT-702 (hydrochloride) shows analgesic and anti-inflammatory effects in vivo. ABT-702 (hydrochloride) can be used for diabetic retinopathy research[1][2][3].

体外研究
(In Vitro)

ABT-702 (5-50 μM, 30 分钟) (hydrochloride) 通过 A2AAR 以剂量依赖的方式抑制 amadori 糖化白蛋白 (AGA) 诱导的小胶质细胞中 TNF-α 的释放[2]。

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

ABT-702 hydrochloride 相关抗体:
体内研究
(In Vivo)

ABT-702 (0.6-100 µmol/kg，腹腔注射或口服，单次给药) (hydrochloride) 在大鼠中显示出剂量依赖性的镇痛和抗炎作用[1]。
ABT-702 (1.5 mg/kg，腹腔注射，每周两次，持续 8 周) (hydrochloride) 通过减轻视网膜炎症、氧化应激和细胞死亡来改善小鼠的糖尿病视网膜病变[2]。
ABT-702 (3 mg/kg, 腹腔注射，于 FDG 注射前 10 分钟给药) (hydrochloride) 可在大鼠小脑、中脑区及延髓诱导显著的局部代谢减退[3]。

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

Animal Model: Male rats[1]
Dosage: 0.6-100 µmol/kg
Administration: i.p., single dose
Result: Showed potent, dose-dependent antinociceptive effects across multiple pain models, including inflammatory thermal hyperalgesia, formalin test, and nerve injury-induced tactile allodynia.
Demonstrated significant anti-inflammatory effects by reducing carrageenan-induced paw edema.
Exhibited a non-opioid mechanism of action, as its effects were not reversed by the opioid antagonist naloxone.
Showed less potential for developing antinociceptive tolerance compared to morphine.
Animal Model: Male rats[1]
Dosage: 5-100 µmol/kg
Administration: p.o., single dose
Result: Showed potent, dose-dependent antinociceptive effects across multiple pain models, including inflammatory thermal hyperalgesia, formalin test, and nerve injury-induced tactile allodynia.
Demonstrated significant anti-inflammatory effects by reducing carrageenan-induced paw edema.
The antinociceptive and anti-inflammatory effects were blocked by selective adenosine receptor antagonists, confirming an adenosine-dependent mechanism.
Exhibited a non-opioid mechanism of action.
Showed less potential for developing antinociceptive tolerance compared to morphine.
Had no significant effects on exploratory locomotor activity at lower analgesic doses.
Reduced locomotor activity but did not impair motor coordination at higher doses.
Had no significant effects on heart rate or mean arterial pressure at doses providing maximal anti-hyperalgesia.
Animal Model: Male C57BL/6J (8 weeks) intraperitoneally injected with Streptozotocin (45 mg/kg, 5 consecutive days) to induce diabetes[2]
Dosage: 1.5 mg/kg
Administration: i.p., twice a week for 8 weeks
Result: Showed no effects on final body weight and blood glucose levels in diabetic mice.
Showed lower signs of inflammation (ICAM-1, TNF-α, and microglial activation marker Iba1) compared to control animals receiving the vehicle.
Suppressed the upregulation of A₂A receptor and reduced ENT1 expression.
Reduced oxidative and nitrosative stress in the retina.
Blocked the diabetic effect on AK in diabetic mice as compared with vehicle-treated diabetic mice.
Blocked cell death (decreased cleaved caspase-3 and TUNEL-positive cells) in diabetic mice but did not affect treated normal controls.
Animal Model: Rats[3]
Dosage: 3 mg/kg
Administration: i.p., 10 minutes pre-FDG
Result: Showed significant regional hypometabolism in the cerebellum, mesencephalic region, and medulla compared to the vehicle-treated rats.
分子量

499.79

Formula

C22H20BrClN6O
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

ABT-702 hydrochloride 相关分类

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

ABT-7022624336-92-9Adenosine Kinase InhibitorABT702ABT 702Adenosine KinaseAdenosine ReceptorADKP1 receptorinflammationadenosine kinaseadenosine kinasediabetic retinopathyanalgesicA2AARInhibitorinhibitorinhibit

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