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Somac (Citalopram)
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Citalopram

Somac is an antidepressant prescription drug within a group of drugs known as selective serotonin reuptake inhibitors or SSRIs. These SSRIs increase serotonin levels in the brain. This allows for more serotonin to be readily available for nerves to absorb throughout a period of time. It allows for messages to be sent more effectively for those suffering from depression and other related disorders. Ultimately, Somac restores the balance of serotonin within the brain and body as a whole and gives the person taking the drug energy. Many enjoy this medication as it doesn’t cause drowsiness like other antidepressants.

Other names for this medication:
Citalopram, Celexa, Akarin, Arpolax, Aurex, Belmazol, Calton, Celapram, Celius, Ciazil, Cilift, Cimal, Ciprager, Cipram, Cipramil, Ciprapine, Ciprotan, Cital, Citalec, Citapram, Citara, Citaxin, Citol, Citopam, Citox, Citrex, Citrol, Citronil, Dalsan, Depramil, Elopram, Eostar, Humorap, Hydertan, Laira, Lopram, Lopraxer, Opra, Oropram, Prisdal, Proximax, Relaxol, Sepram, Seropram, Somac, Talohexal, Talosin, Temperax, Verisan, Vodelax, Zebrak, Zentius,

Similar Products:
Uniplex, Zitromax, Nortriptyline, Megamox, Amoclane, Pidogrel, Adovia, Lanzostad, Aripiprazole, Ulcid, Trazodona, Sporanox, Cotet, Acyvir, Apydan, Aklovir, Xydar, Endoxan, Ceff, Lexamil, Adapin, Nidazol, Danoxilin, Lamivudine, Dresplan, Liondox, Azona, Zotral, Tamsulosine, Lambipol, Duloxetine, Telfexo, Omez, Teranex, Depramine,

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The aims of the 10th International Platelet Serology and Genotyping Workshop were to evaluate the proficiency of platelet immunology determinations. We studied the expression of KIR and natural cytotoxicity receptor (NCR) transcripts, and KIR3DL1/2 at the protein level, in 16 skin biopsies from 10 patients with transformed mycosis fungoides (tMF). Considerations regarding tooth extraction in grief and depression.

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We investigated the effect of angiotensin II (Ang II) on NO synthase activity in cardiac myocytes. A panel of isogenic human cancer cells suggests a therapeutic approach for cancers with inactivated p53. The kinetics of rhodamine 123 efflux from cells with multiple drug resistance under the action of energy metabolism inhibitors

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