N6-Cyclohexyladenosine (CHA)
(Synonyms: A1受体促进剂,CHA,CHA) 目录号 : GC33667
An A1 adenosine receptor agonist
Cas No.:36396-99-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
N6-Cyclohexyladenosine is an adenosine receptor agonist.1 It selectively binds to adenosine A1 receptors in rat cortical membranes (IC50 = 2.3 nM) over A2 receptors in rat striatal membranes (IC50 = 870 nM). N6-Cyclohexyladenosine decreases heart rate and increases coronary flow in a perfused working rat heart model ex vivo (EC25s = 5 and 860 nM, respectively). In vivo, it decreases heart rate and blood pressure in normotensive rats (EC25s = 2.4 and 4.2 μg/kg, respectively).1 N6-Cyclohexyladenosine (100 μM) induces sleep in rats when administered via basal forebrain infusion.2 N6-Cyclohexyladenosine also decreases locomotor activity in mice (ED50 = 60 μg/kg, i.p.).3
1.Hutchison, A.J., Webb, R.L., Oei, H.H., et al.CGS 21680C, an A2 selective adenosine receptor agonist with preferential hypotensive activityJ. Pharmacol. Exp. Ther.251(1)47-55(1989) 2.Blanco-Centurion, C., Xu, M., Murillo-Rodriguez, E., et al.Adenosine and sleep homeostasis in the basal forebrainJ Neurosci.26(31)8092-8100(2006) 3.Nikodijevi?, O., Daly, J.W., and Jacobson, K.A.Characterization of the locomotor depression produced by an A2-selective adenosine agonistFEBS Lett.261(1)67-70(1990)
| Cas No. | 36396-99-3 | SDF | |
| 别名 | A1受体促进剂,CHA,CHA | ||
| Canonical SMILES | OC[C@@H]1[C@H]([C@H]([C@H](N2C=NC3=C2N=CN=C3NC4CCCCC4)O1)O)O | ||
| 分子式 | C16H23N5O4 | 分子量 | 349.38 |
| 溶解度 | DMSO : ≥ 100 mg/mL (286.22 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.8622 mL | 14.3111 mL | 28.6221 mL |
| 5 mM | 0.5724 mL | 2.8622 mL | 5.7244 mL |
| 10 mM | 0.2862 mL | 1.4311 mL | 2.8622 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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Further characterization of the renovascular effects of N6-cyclohexyladenosine in the isolated perfused rat kidney
J Pharmacol Exp Ther 1987 Mar;240(3):911-5.PMID:3559983doi
Previous studies have shown that activation of A1 adenosine receptors results in renal vasoconstriction at submicromolar concentrations of N6-Cyclohexyladenosine (CHA) followed by relative vasodilation at higher concentrations. The present data confirm these findings and demonstrate that Na loading enhances the vasoconstrictor effects of CHA in the isolated rat kidney perfused at constant flow. Furthermore, adenosine receptor antagonism with both theophylline and the A1-selective antagonist, xanthine amine congener (8-[4-[(2-aminoethyl)-aminocarbonylmethyloxy]phenyl]-1, 3-dipropylxanthine), produced a rightward and apparently parallel shift in the dose response to CHA. Determination of the inhibitory constants for both antagonists revealed that xanthine amine congener was three orders of magnitude more potent than theophylline in antagonizing CHA-induced renal vasoconstriction. Other investigators have hypothesized that angiotensin II mediates adenosine-induced renal vasoconstriction. However, we have been able to show that A1 receptor activation can result in renal vasoconstriction in the isolated perfused rat kidney devoid of renin substrate. Moreover, a competitive inhibitor of angiotensin II (saralasin) failed to attenuate the hemodynamic effects of CHA at doses that completely blocked the effects of angiotensin II itself. Taken together, these data are consistent with the hypothesis that A1 receptor activation in the kidney leads to vasoconstriction, a response that is enhanced by Na loading, and that A1 adenosine receptors and angiotensin II receptors are separate and distinct biochemical entities. Independent activation of either receptor leads to renal vasoconstriction, which can be prevented by its respective antagonist.
Adenosine A1 receptor agonist, N6-cyclohexyladenosine, protects myelin and induces remyelination in an experimental model of rat optic chiasm demyelination; electrophysiological and histopathological studies
J Neurol Sci 2013 Feb 15;325(1-2):22-8.PMID:23260322DOI:10.1016/j.jns.2012.11.008.
Chronic demyelinated lesions and subsequent functional impairment are resulted from eventual failure of remyelination process as seen in multiple sclerosis. Activation of adenosine A1 receptor is reported to be effective on neural stem cells (NSCs) proliferation and oligodendrocytes differentiation. Therefore, this study attempted to investigate the effect of A1 receptor agonist N6-Cyclohexyladenosine (CHA), on lysolecithin (LPC) induced demyelination and remyelination in rat optic chiasm. The experiments were carried out on male Wistar rats using visual evoked potential recording, myelin staining by Luxol fast blue and histological evaluation of demyelinated and remyelinated axons within the area of lesion. CHA was administrated i.c.v. during demyelination or remyelination phases. As revealed by myelin staining, the most extent of demyelination occurred at 7th day post-lesion (dpl 7), but gradually myelination was restored toward control during days 14-28. VEP P1-latency and P1-N1 amplitude showed widespread demyelination on dpl 7 and 14 which consequently was reversed during days 14-28 post lesion. I.c.v. treatment of animals with CHA during demyelination phase (days 0-13) reduced the extent of demyelination. During remyelination phase (days 14-28), CHA was able to increase remyelination in both electrophysiological and histopathological studies. The effects of CHA seem to be due to its protective effect on myelinating cells and its regenerative effect through potentiating endogenous neural progenitors.
Inhibition of N6-[3H]cyclohexyladenosine binding by carbamazepine
Epilepsia 1990 Sep-Oct;31(5):503-12.PMID:2401242DOI:10.1111/j.1528-1157.1990.tb06098.x.
The mechanism of action of carbamazepine (CBZ) (Tegretol), despite widespread use in the management of partial and tonic-clonic seizures in adults, is not completely understood. In animals, adenosine and adenosine analogues have anticonvulsant effects that may be due to interactions with central A1 adenosine receptors. CBZ (at therapeutically relevant concentrations) inhibits the binding of agonists and antagonists to brain A1 adenosine receptors, but whether as an agonist/antagonist is not clear. The adenosine agonist, N6-[3H]cyclohexyladenosine ([3H]CHA), binds to membranes from rat cortex and hippocampus at two nanomolar binding sites or states. To clarify the actions of carbamazepine at the A1 adenosine receptor, its inhibitory actions were compared with those of known adenosine agonists and xanthine antagonists using 0.1 nM[3H]CHA, in which almost all binding is to the higher affinity state, or 10 nM [3H]CHA, in which there is a substantial contribution of binding from both states. The ratios of the IC50 values (concentration that inhibits specific binding by 50%) at 10 nM [3H]CHA to the IC50 values at 0.1 nM [3H]CHA were 18-31 for the agonists and 4-10 for the xanthine antagonists. CBZ had a ratio of 3. The inhibitory effects of GTP on [3H]CHA binding were less in the presence of the adenosine agonist, 2-chloroadenosine than were inhibitory effects in the presence of the xanthine antagonist theophylline or CBZ in both cortex and hippocampus. These in vitro studies indicate that CBZ is an antagonist at A1 adenosine receptors in cerebral cortical and hippocampal membranes from rat brain. Agonist activity at A1 adenosine receptors would have been compatible with the sedative anticonvulsant effects of CBZ, but these data do not support a role of the anticonvulsant action of carbamazepine on A1 adenosine receptors in cerebral cortex or hippocampus.
The effect of N6-Cyclohexyladenosine and 5'-N-ethylcarboxamidoadenosine on body temperature in normothermic rabbits
Gen Pharmacol 1996 Apr;27(3):467-9.PMID:8723528DOI:10.1016/0306-3623(95)00098-4.
1. Thermal responses to i.v. administration of N6-Cyclohexyladenosine (CHA; 0.15 mg/kg), A1 adenosine receptor agonist, or 5'-N-ethylcarboxamidoadenosine (NECA; 0.15 mg/kg), A2 adenosine receptor agonist, were investigated in normothermic rabbits at an ambient temperature (Ta) of 20.0 +/- 1.0 degrees C. 2. Although both compounds inhibited metabolic heat production, only NECA produced hypothermia. 3. NECA showed strong hypotensive activity. 4. Both compounds produced vasoconstriction of the ear skin vessels and CHA, in addition, slowed down the respiratory rate. 5. The role of A1 or A2 adenosine receptors in the thermoregulatory activity of these compounds is discussed.
Modulation of conventional outflow facility by the adenosine A1 agonist N6-Cyclohexyladenosine
Invest Ophthalmol Vis Sci 2005 Oct;46(10):3795-9.PMID:16186365DOI:10.1167/iovs.05-0421.
Purpose: Studies have shown that the activation of adenosine A(1) receptors lower intraocular pressure primarily by increasing total outflow facility. The purpose of this study was to investigate the actions of the adenosine A(1) agonist N(6)-cyclohexyladenosine (CHA) on conventional outflow facility. Methods: Conventional outflow facility was evaluated in isolated bovine anterior segments, perfused at a constant pressure of 10 mm Hg. After overnight perfusion to establish a stable baseline, the concentration- and time-dependent changes in outflow facility induced by CHA were determined. To confirm the involvement of adenosine A(1) receptors and matrix metalloproteinases (MMP) in any change in facility, the responses to CHA were evaluated in preparations treated with the adenosine A(1) receptor antagonist, 8-cyclopentyl-1,3-dimethylxanthine (CPT), or the nonselective MMP inhibitor GM-6001. Results: The administration of CHA (10 microM) to perfused anterior segments produced a 28% increase in outflow facility over basal levels. This response was relatively slow to develop with no significant change in outflow facility measured until after 60 minutes of CHA infusion. The peak response to CHA infusion occurred between 3 and 4 hours after CHA administration. Analysis of the CHA concentration-response curves demonstrated that this increase in outflow facility was concentration-dependent, with an EC(50) of 0.28 microM. Pretreatment with the adenosine A(1) receptor antagonist CPT (10 microM) or the nonselective MMP inhibitor GM-6001 (10 microM) blocked the response to CHA (1 microM). When compared with control eyes, no significant change in baseline facility was measured in eyes perfused with CPT or GM-6001. Conclusions: These studies demonstrate that the adenosine agonist CHA significantly increases conventional outflow facility in the perfused bovine eye. Analysis of the CHA concentration-response curve and inhibition of the CHA-induced increase in outflow facility by the adenosine A(1) antagonist confirms that this response is mediated by the activation of adenosine A(1) receptors. The inhibition of the CHA-induced increase in outflow facility by the MMP inhibitor GM-6001 provides evidence that the secretion and activation of MMPs within the conventional outflow pathway play a central role in the ocular hypotensive action of adenosine A(1) agonists.