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

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

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ABT-702

ABT-702 Chemical Structure

CAS No. : 214697-26-4

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Based on 3 publication(s) in Google Scholar

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ABT-702 Related Antibodies

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

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Description

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

IC50 & Target

IC50: 1.7 nM (Adenosine kinase, AK)[1]
In Vitro

ABT-702 (5-50 μM, 30 min) inhibits amadori-glycated-albumin (AGA)-induced TNF-α release in a dose-dependent manner in AGA-treated microglial cells via the adenosine A2AA receptor (A2AAR)[2].

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

ABT-702 Related Antibodies
In Vivo

ABT-702 (0.6-100 µmol/kg, i.p. or p.o., single dose) shows dose-dependent analgesic and anti-inflammatory effects in rats[1].
ABT-702 (1.5 mg/kg, i.p., twice a week for 8 weeks) meliorates diabetic retinopathy in mice by attenuating retinal inflammation, oxidative stress, and cell death[2].
ABT-702 (3 mg/kg, i.p., 10 minutes pre-FDG) induces significant regional hypometabolism in the cerebellum, mesencephalic region, and medulla in rats[3].

MedChemExpress (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.
Molecular Weight

463.33

Formula

C22H19BrN6O
CAS No.
SMILES

BrC1=CC=CC(C2=C3C(N)=NC=NC3=NC(C4=CC=C(N5CCOCC5)N=C4)=C2)=C1
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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ABT-702 Related Classifications

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Help & FAQs
  • 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-702214697-26-4ABT702ABT 702Adenosine KinaseAdenosine ReceptorADKP1 receptoradenosine kinasediabetic retinopathyanalgesicA2AARInhibitorinhibitorinhibit

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