1. Neuronal Signaling
  2. Serotonin Transporter
  3. CM 57373

CM 57373 is an orally active anorectic agent. CM 57373 releases serotonin and inhibits serotonin reuptake in rat brain synaptosomes. CM 57373 reduces food intake, decreases body weight and alleviates experimentally induced hyperphagia. CM 57373 can be used in obesity research.

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CM 57373

CM 57373 Chemical Structure

CAS No. : 98644-22-5

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Description

CM 57373 is an orally active anorectic agent. CM 57373 releases serotonin and inhibits serotonin reuptake in rat brain synaptosomes. CM 57373 reduces food intake, decreases body weight and alleviates experimentally induced hyperphagia. CM 57373 can be used in obesity research[1][2].

In Vitro

CM 57373 inhibits serotonin reuptake and releases serotonin in rat brain synaptosomes in vitro[1].
CM 57373 exhibits very low affinity for serotonin receptors in rat brain membranes in vitro, with potency less than one-hundredth that of m-chlorophenylpiperazine[1].

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

In Vivo

CM 57373 (0.1-20 mg/kg; i.p.) dose-dependently decreases brain 5-HIAA concentrations in healthy male Sprague-Dawley rats, with significant reductions observed at doses ≥5 mg/kg i.p., and produces no consistent significant changes in brain serotonin concentrations[1].
CM 57373 (2.5-20 mg/kg; i.p.) antagonizes p-chloroamphetamine-induced brain serotonin depletion in healthy male Sprague-Dawley rats with an ED50 of 7 mg/kg, achieving complete restoration at a 20 mg/kg i.p. dose[1].
CM 57373 hydrochloride (3.75-15 mg/kg; p.o.; single dose) produces a dose-dependent anorectic effect in food-deprived female Sprague-Dawley rats with an oral ID50 of 7.4 mg/kg[2].
CM 57373 (1.25-10 mg/kg; p.o.; single dose) produces a dose-dependent anorectic effect in male and female Beagle dogs with an oral ID50 of 2.4 mg/kg and good tolerability[2].
CM 57373 (3-7.5 mg/kg; p.o.; single dose, daily via drinking water; 16 days) reduces cafeteria-diet hyperphagia in female Sprague-Dawley rats, with tolerance developing over 16 days; it lowers telencephalic 5-HIAA levels without altering 5-HT levels and sustains reduced body weights despite tolerance[2].
CM 57373 (7.5 mg/kg; p.o.; single dose) prevents insulin-induced hyperphagia in female Sprague-Dawley rats without altering insulin-induced hypoglycemia[2].

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

Animal Model: Sprague-Dawley (male, 180-220 g)[1]
Dosage: 0.1 mg/kg; 1 mg/kg; 5 mg/kg; 10 mg/kg; 20 mg/kg
Administration: i.p.
Result: Decreased brain 5-HIAA concentrations to 1.13 nmol/g, 1.10 nmol/g, and 0.98 nmol/g at 4 hours after 5 mg/kg, 10 mg/kg, and 20 mg/kg doses respectively (control = 1.65 nmol/g).
Produced no significant changes in brain serotonin concentrations at 4 hours after 5 mg/kg, 10 mg/kg, or 20 mg/kg doses.
Caused a small decrease in brain serotonin concentrations at 4 and 8 hours after 10 mg/kg dose, which was not consistent across studies.
Failed to produce significant effects on brain serotonin or 5-HIAA concentrations at 4 hours after 0.1 mg/kg or 1 mg/kg doses.
Reduced brain 5-HIAA concentrations within 1 hour after 10 mg/kg dose, with continued decrease up to 8 hours and recovery to control levels by 24 hours.
Animal Model: Sprague-Dawley (male, 180-220 g)[1]
Dosage: 2.5 mg/kg; 5 mg/kg; 10 mg/kg; 20 mg/kg
Administration: i.p.
Result: Antagonized p-chloroamphetamine-induced brain serotonin depletion in a dose-dependent manner.
Restored brain serotonin concentrations to control levels (~3 nmol/g) after 20 mg/kg dose, achieving complete antagonism.
Had an estimated ED50 value of 7 mg/kg for antagonizing p-chloroamphetamine-induced brain serotonin depletion.
Animal Model: Sprague-Dawley (female, 175-200 g)[2]
Dosage: 3.75 mg/kg; 7.5 mg/kg; 15 mg/kg
Administration: p.o.; single dose
Result: Caused a dose-related reduction in food consumption.
Achieved an oral ID50 of 7.4 mg/kg.
Animal Model: Beagle (male and female, 11-14 kg, 5-10 per group)[2]
Dosage: 1.25 mg/kg; 2.5 mg/kg; 5 mg/kg; 10 mg/kg
Administration: p.o.; single dose
Result: Caused a dose-related reduction in food consumption.
Achieved an oral ID50 of 2.4 mg/kg.
Was well tolerated, with only moderate mydriasis observed at the 10 mg/kg dose.
Animal Model: Sprague-Dawley (female, initial weight 254 g)[2]
Dosage: 7.5 mg/kg (single dose on day 1, 8, and 16); 3 mg/kg (daily via drinking water for 16 days)
Administration: p.o.; single dose (day 1, 8, 16); daily via drinking water; 16 days
Result: Reduced 6-hour cafeteria food consumption to 5.03 g (52% of vehicle control levels, P < 0.01) on day 1.
Reduced 6-hour cafeteria food consumption to 8.00 g (56% of vehicle control levels, P < 0.01) on day 8.
Reduced 6-hour cafeteria food consumption to 9.70 g (76% of vehicle control levels, no significant difference from vehicle) on day 16.
Developed tolerance to the anorectic effect over 16 days, which was less pronounced on day 8 compared to dl-fenfluramine.
Lowered body weights early and maintained them below vehicle controls throughout the treatment period.
Did not modify telencephalic 5-HT levels on any day.
Reduced telencephalic 5-HIAA levels to 328 ng/g (day 1, P < 0.01), 236 ng/g (day 8, P < 0.01), and 305 ng/g (day 16, P < 0.01) relative to vehicle controls.
Animal Model: Sprague-Dawley (female, 175-200 g)[2]
Dosage: 7.5 mg/kg
Administration: p.o.; single dose
Result: Reduced 1-hour food intake to 0.73 g in saline-treated rats (P < 0.05 vs. vehicle).
Reduced 1-hour food intake to 0.47 g in insulin-treated rats (P < 0.01 vs. vehicle), preventing the insulin-induced increase in food intake.
Did not modify insulin-induced hypoglycemia, with plasma glucose levels of 51 mg% (vs. 45 mg% in insulin-only controls).
Molecular Weight

256.15

Formula

C10H14BrN3

CAS No.
SMILES

BrC=1N=C(C=CC1)N2CCC(N)CC2

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CM 57373
Cat. No.:
HY-184316
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