For research use only. Not for therapeutic Use.
MK-212 HCl (CAT: I008053) is a selective serotonin receptor agonist that primarily targets the 5-HT2C receptor subtype. It acts as a partial agonist at 5-HT2C receptors and has a weaker affinity for other serotonin receptor subtypes. MK-212 HCl has been used in preclinical and clinical research to study the role of 5-HT2C receptors in various physiological and behavioral processes, including mood regulation, appetite control, and cognitive function.
Catalog Number | I008053 |
CAS Number | 61655-58-1 |
Synonyms | MK212; MK 212; MK-212;2-chloro-6-(piperazin-1-yl)pyrazine hydrochloride |
Molecular Formula | C8H12Cl2N4 |
Purity | ≥95% |
Target | Neuronal Signaling |
Solubility | Soluble in DMSO, not in water |
Storage | Store at RT |
IUPAC Name | 2-chloro-6-piperazin-1-ylpyrazine;hydrochloride |
InChI | InChI=1S/C8H11ClN4.ClH/c9-7-5-11-6-8(12-7)13-3-1-10-2-4-13;/h5-6,10H,1-4H2;1H |
InChIKey | PFIZGLUIYAZQFU-UHFFFAOYSA-N |
SMILES | C1CN(CCN1)C2=CN=CC(=N2)Cl.Cl |
Reference | 1:J Pharmacol Exp Ther. 1993 Aug;266(2):836-44. Long-term treatment with the antidepressants fluoxetine and desipramine potentiates endocrine responses to the serotonin agonists 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) and (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI).Li Q,Brownfield MS,Battaglia G,Cabrera TM,Levy AD,Rittenhouse PA,van de Kar LD, PMID: 8394920 </br><span>Abstract:</span> Various endocrine responses to 5-hydroxytryptamine (serotonin, 5-HT) agonists were used to assess serotonergic receptor function after chronic treatment with the antidepressants fluoxetine (10 mg/kg), a 5-HT uptake blocker and the norepinephrine uptake blocker desipramine (DMI, 5 mg/kg). Both were injected (i.p.) once a day for 21 days. DOI (5-HT1C/2 agonist, 0-5 mg/kg i.p.) and 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) (less selective, but predominantly a 5-HT1C agonist, 0-20 mg/kg i.p.) were administered 18 hr after the final antidepressant injection and 30 min before decapitation. Chronic treatment with both fluoxetine and DMI produced a potentiation in most hormone responses to the 5-HT agonists (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane HCl (DOI) and MK-212, although there were several differences in individual hormone responses to the two 5-HT agonists. Fluoxetine and DMI potentiated the MK-212- and DOI-induced increase of plasma oxytocin levels and potentiated the effect of DOI on plasma adrenocorticotropic hormone (corticotropin) and prolactin levels. In contrast, the effect of the high dose of MK-212 on plasma prolactin concentration was reduced by both antidepressants. Only MK-212 increased vasopressin levels and this effect was potentiated by fluoxetine, but not by DMI. Fluoxetine also significantly increased the resting level of plasma vasopressin. DMI potentiated the effect of MK-212 on plasma renin concentration. Pretreatment with fluoxetine significantly increased (38%) the Bmax for the 5-HT1C/2 agonist sites ([125I]DOI) in the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS) |