2-Chloroadenosine

2-Chloroadenosine is an adenosine analog, a transporter permeabilizer of nucleoside transporters, and a competitive uridine influx inhibitor (apparent K_i=33 μM). 2-Chloroadenosine binds to nitrobenzylthioinosine with high affinity (apparent K_i=0.18 mM). 2-Chloroadenosine promotes Apoptosis and increases cerebral blood flow. 2-Chloroadenosine has anticonvulsant properties. 2-Chloroadenosine is used to study infection, inflammatory diseases, cancer, blood-related diseases, lung injury, epilepsy, and kidney disease^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17]}. In Vitro:2-Chloroadenosine (50 μM; 24-72 h) can lead to increased apoptosis, cell cycle arrest in the S phase, inhibition of DNA synthesis, and DNA strand breaks in PC3 cells^[1].
2-Chloroadenosine (10-50 μM, 6-72 h) induces apoptotic cell death in EHEB cells^[2].
2-Chloroadenosine (0.01-1.0 mM; 18 h) has a selective lethal effect, leading to a rapid decrease in intracellular ATP content in mouse peritoneal macrophages^[6].
In Vivo:2-Chloroadenosine (15 nmol; local injection; multiple doses, before ischemia, 4 h and 10 h after reperfusion; 7 days) protects hippocampal CA₁ neurons from ischemic cell loss in a rat model of incomplete forebrain ischemia-reperfusion^[7].
2-Chloroadenosine (0.3-12 nmoles; intraparenchymal injection; single dose) produces dose-dependent and sustained cerebral vasodilation and increases cerebral blood flow in normal rats as measured by spin-labeled MRI, with significant effects on both local and hemispheric blood flow^[8].
2-Chloroadenosine (0.5-4 mg/kg, i.p.) inhibits the shake response in rats induced by ice-water exposure, Icilin (HY-11062) injection, or Naloxone (HY-17417A)-precipitated morphine withdrawal in a dose-dependent manner^[9].
2-Chloroadenosine (1-10 mg/kg; intraperitoneal injection; administered after the first successful stimulation) has different degrees of inhibitory effects on cortical postepileptic discharges in rats of different ages, and the inhibitory effects on movement and EEG phenomena are most obvious in 18-day-old rats^[10].
2-Chloroadenosine (1 mg/mL; intravenous infusion) can alleviate rabbit lung ischemia-reperfusion injury, reduce pulmonary artery pressure, increase cardiac output, and reduce alveolar leukocyte infiltration and protein exudation^[11].
2-Chloroadenosine (9-18 nM/min; intravenous injection) can reduce mean arterial blood pressure, filtration fraction, inulin clearance, urine flow and K excretion rate in anesthetized rats in a dose-dependent manner, while reducing Na excretion rate and fractional Na excretion, and increasing plasma K^[12].
2-Chloroadenosine (0.1 mM; local perfusion) increases collateral-dependent and normal cerebral blood flow in canine middle cerebral artery branch occlusion^[13].
2-Chloroadenosine (0.25-1 mg/kg; intraperitoneal injection) significantly increases the electroconvulsive threshold and enhances the anticonvulsant activity of carbamazepine and clonazepam in mice^[14].
2-Chloroadenosine (10 μg/kg/day; intravenous injection; 5 days) improves the survival rate of BALB/c mice infected with Klebsiella pneumoniae B5055 and reduces the levels of inflammatory markers^[15].
2-Chloroadenosine (10 μg/kg; intravenous injection) can alleviate acute lung injury induced by live Escherichia coli or endotoxin plus latex particles in guinea pigs under neutropenia and reduce plasma TNF-α levels^[16].