2. Membrane Transporter/Ion Channel Neuronal Signaling
  3. nAChR
  4. Altinicline

Altinicline (SIB-1508Y free base) is a selective α4β2 nicotinic acetylcholine receptor (nAChR) agonist, with no activity against α7 or α1β1γδ nAChRs and only extremely low activity against α3β4 nAChRs. Altinicline reverses escape deficits and increases avoidance responses. Altinicline is applicable to research related to depression.

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Altinicline

Altinicline Chemical Structure

CAS No. : 179120-92-4

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Description

Altinicline (SIB-1508Y free base) is a selective α4β2 nicotinic acetylcholine receptor (nAChR) agonist, with no activity against α7 or α1β1γδ nAChRs and only extremely low activity against α3β4 nAChRs. Altinicline reverses escape deficits and increases avoidance responses. Altinicline is applicable to research related to depression[1].

In Vivo

Altinicline (0.375-1.5 mg/kg/day; s.c.; subchronic: 5 consecutive days, chronic: 4 weeks prior plus 5 days post-testing start) produces significant, long-lasting reversal of inescapable shock-induced escape failures in the learned helplessness rat model of depression, with additional enhancement of avoidance learning, via a nicotinic acetylcholine receptor-mediated mechanism[1].

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

Animal Model: Sprague-Dawley (male, 200-240 g, learned helplessness model induced by inescapable footshocks)[1]
Dosage: 0.375 mg/kg/day; 0.75 mg/kg/day; 1.5 mg/kg/day (subchronic); 1.5 mg/kg/day (chronic)
Administration: s.c.; subchronic: 5 consecutive days (single bolus on day 1, split doses days 2-5); chronic: 4 weeks daily bolus prior to testing, plus split doses days 2-5 post-testing start
Result: Produced dose-dependent reversal of inescapable shock-induced escape failures at 1.5 mg/kg/day subchronic treatment: session 1 escape failures = 10, session 2 = 4, session 3 = 5, session 4 = 5 (all significantly different from vehicle controls, P<0.05).
Produced significant session-dependent increase in avoidance responding in inescapable shock rats at 1.5 mg/kg/day subchronic treatment, with statistically significant elevations in sessions 2, 3, and 4 compared to vehicle controls.
Produced no significant effect on intertrial crossings or shock sensitivity with subchronic treatment.
Significantly reversed escape failures in inescapable shock rats at 1.5 mg/kg/day chronic treatment: session 1 escape failures = 10, session 2 = 5, session 3 = 5, session 4 = 3 (all significantly different from vehicle controls, P<0.05).
Produced significant increase in avoidance responding at 1.5 mg/kg/day chronic treatment: session 4 = 10 responses, compared to 0 in vehicle controls.
Significantly increased intertrial crossings in sessions 2 and 4 compared to vehicle controls with 1.5 mg/kg/day chronic treatment.
Blocked escape failure reversal effect of subchronic 1.5 mg/kg/day treatment by co-administration of 6 mg/kg/day mecamylamine.
Retained antidepressant-like effects (escape failure reversal) for 1 week following cessation of drug administration.
Molecular Weight

186.26

Formula

C12H14N2
CAS No.
SMILES

CN1[C@@H](CCC1)C=2C=C(C#C)C=NC2
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References
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Keywords:

Altinicline179120-92-4SIB-1508YnAChRNicotinic acetylcholine receptorsratsdepressionhuman α4β2 nicotinic acetylcholine receptorα1β1γδ nicotinic acetylcholine receptorlearned helplessness rat modelα3β4 nicotinic acetylcholine receptorα7 nicotinic acetylcholine receptormecamylamineInhibitorinhibitorinhibit

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