- Sertraline
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- $0.00 / 1Kg/Bag
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2026-01-16
- CAS:79617-96-2
- Min. Order: 1Kg/Bag
- Purity: USP, GMP
- Supply Ability: 20tons
- Sertraline Free Base
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- $1520.00 / 25mg
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2026-01-05
- CAS:79617-96-2
- Min. Order:
- Purity:
- Supply Ability: 10g
- Sertraline
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- $0.00 / 10mg
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2026-01-04
- CAS:79617-96-2
- Min. Order: 10mg
- Purity: 79617-96-2
- Supply Ability: 100kg
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| | Sertraline Basic information |
| Product Name: | Sertraline | | Synonyms: | (1s-cis)-1,2,3,4-tetrahydro-4-(3,4-dichlorophenyl)-n-methyl-1-naphthalenamin;1,2,3,4-tetrahydro-4-(3,4-dichlorophenyl)-n-methyl-1-naphthalenamin(1s-cis;cp51974;(1s,4s)-4-(3,4-dichlorophenyl)-n-methyl-1,2,3,4-tetrahydro-1-naphthalenamine;(1s-cis)-4-(3,4-dichlorophenyl)-1,2,3,4-tetrahydro-n-methyl-1-naphthalenamine;SERTRALINE;4(3,4-dichlorophenyl)1,2,3,4 tetrahydro-N-methyl-1-naphthalenamine (cis-racemate) (intermediate of sertraline hcl);(1S,4R)-4-(3,4-dichlorophenyl)-N-methyl-tetralin-1-amine | | CAS: | 79617-96-2 | | MF: | C17H17Cl2N | | MW: | 306.23 | | EINECS: | 605-001-5 | | Product Categories: | API;Amines;(intermediate of sertraline hcl);Sertraline;79617-96-2 | | Mol File: | 79617-96-2.mol |  |
| | Sertraline Chemical Properties |
| Boiling point | 416.3±45.0 °C(Predicted) | | density | 1.25±0.1 g/cm3(Predicted) | | pka | pKa 9.48±0.04(H2O
I > 0)(Approximate) | | Water Solubility | <0.1g/L(room temperature) | | InChI | InChI=1S/C17H17Cl2N/c1-20-17-9-7-12(13-4-2-3-5-14(13)17)11-6-8-15(18)16(19)10-11/h2-6,8,10,12,17,20H,7,9H2,1H3/t12-,17-/m0/s1 | | InChIKey | VGKDLMBJGBXTGI-SJCJKPOMSA-N | | SMILES | [C@@H]1(NC)C2=C(C=CC=C2)[C@H](C2=CC=C(Cl)C(Cl)=C2)CC1 | | CAS DataBase Reference | 79617-96-2(CAS DataBase Reference) | | NIST Chemistry Reference | Sertraline(79617-96-2) | | EPA Substance Registry System | Sertraline (79617-96-2) |
| | Sertraline Usage And Synthesis |
| Originator | Lustral,Pfizer,UK | | History | The history of sertraline dates back to the early 1970s when Pfizer chemist Reinhard Sarges invented a novel series of psychoactive compounds, including lometraline, based on the structures of the neuroleptics thiothixene and pinoxepin. Further work on these compounds led to tametraline, a norepinephrine and weaker dopamine reuptake inhibitor. A few years later, in 1977, pharmacologist Kenneth Koe, after comparing the structural features of a variety of reuptake inhibitors, became interested in the tametraline series. He asked another Pfizer chemist, Willard Welch, to synthesize some previously unexplored tametraline derivatives. Welch generated several potent norepinephrine and triple reuptake inhibitors, but to the surprise of the scientists, one representative of the generally inactive cis-analogs was a serotonin reuptake inhibitor. Welch then prepared stereoisomers of this compound, which were tested in vivo by animal behavioral scientist Albert Weissman. The most potent and selective (+)-isomer[a] was taken into further development and eventually named sertraline. | | Uses | cis-Sertraline is an isomer of Sertraline. Sertraline is a selective serotonin reuptake inhibitor. It is used as an antidepressant. | | Uses | Antidepressant;5-HT uptake inhibitor | | Definition | ChEBI: A member of the class of tetralins that is tetralin which is substituted at positions 1 and 4 by a methylamino and a 3,4-dichlorophenyl group, respectively (the S,S diastereoisomer). A selective serotonin-reuptake inhibito
(SSRI), it is administered orally as the hydrochloride salt as an antidepressant for the treatment of depression, obsessive-compulsive disorder, panic disorder and post-traumatic stress disorder. | | Brand name | Zoloft (Pfizer). | | Therapeutic Function | Antidepressant | | Biological Functions | Sertraline (Zoloft) has an elimination half-life of 25
hours and can be administered once a day, usually in the
morning to avoid insomnia. Sertraline undergoes extensive
hepatic metabolism, and doses must be reduced in
patients with liver disease. Sertraline may produce more
gastrointestinal side effects, such as nausea and diarrhea,
than does fluoxetine and is generally thought to be
less activating than fluoxetine. It is highly bound to
serum proteins (98%) and may alter plasma protein
binding of other medications.A 14-day washout period
is recommended before starting a MAOI. Sertraline is a
weak inhibitor of cytochrome P450 2D6. Intensive therapeutic
drug monitoring is indicated when combining
sertraline with drugs metabolized by this route that
have a narrow therapeutic index, such as the TCAs and
the type 1C antiarrhythmics propafenone, encainide,
and flecainide. | | General Description | Inspection of sertraline (Zoloft) (1S,4S) reveals the pharmacophorefor SERT inhibition. The Cl substituents alsopredict tropism for a 5-HT system. The depicted stereochemistryis important for activity. | | Pharmaceutical Applications | Sertraline (brand name Zoloft) was approved by the US Food and Drug Administration (FDA) in 1991 based on the recommendation of the Psychopharmacological Drugs Advisory Committee; it had already become available in the United Kingdom the previous year. The FDA committee achieved a consensus that sertraline was safe and effective for the treatment of major depression.
Until 2002, sertraline was only approved for use in adults ages 18 and over; that year, it was approved by the FDA for use in treating children aged 6 or older with severe OCD. In 2005, the FDA added a boxed warning concerning pediatric suicidal behavior to all antidepressants, including sertraline. In 2007, labeling was again changed to add a warning regarding suicidal behavior in young adults ages 18 to 24. | | Mechanism of action | Sertraline is a potent and selective inhibitor of the neuronal reuptake 5-HT transporter. In vitro binding
studies suggest that sertraline has a substantially higher selectivity for inhibiting 5-HT reuptake than other
SSRIs or TCAs, including clomipramine. It has only weak effects on neuronal uptake of NE and
dopamine. Its mechanism of action is common to the SSRIs. Sertraline is very selective, lacking affinity for
other neuroreceptors at therapeutic concentrations. | | Pharmacokinetics | Sertraline appears to be slowly but well absorbed from the GI tract following oral administration. The oral
bioavailability of sertraline in humans ranges from 20 to 36%, suggesting extensive first-pass metabolism to its N-desmethylated metabolite. Food enhances its oral absorption decreasing the time to
achieve peak plasma concentrations from approximately 8 to 6 hours. Following multiple dosing, steady-state
plasma sertraline concentrations are proportional and linearly related to dose (half-life: single dose, 24
hours; multiple dose, 24 hours). N-desmethylsertraline, sertraline's principal metabolite, exhibits
dose-dependent pharmacokinetics. Sertraline and N-desmethylsertraline are distributed into breast milk.
Although in elderly patients the elimination half-life is increased to approximately 36 hours, this effect does
not appear to be clinically important and does not warrant dosing alterations. Sertraline is primarily
metabolized by CYP3A4 N-demethylation in the intestine and liver to its principal metabolite
N-desmethylsertraline and several other metabolites. N-desmethylsertraline is approximately 5- to 10 times
less potent as an inhibitor of 5-HT reuptake than sertraline. Sertraline and N-desmethylsertraline undergo
further metabolism via oxidative deamination and ring hydroxylation and glucuronide conjugation.
N-desmethylsertraline has an elimination half-life approximately 2.5 times that of sertraline. Following oral
administration, sertraline and its conjugated metabolites are excreted in both urine and feces, and
unmetabolized sertraline accounts for less than 5% of oral dose. Plasma clearance of sertraline was
approximately 40% lower in geriatric patients. The elimination half-life of sertraline in patients with hepatic
disease was prolonged to a mean of 52 hours, compared with 22 hours in individuals without hepatic disease. | | Clinical Use | SSRI:
Antidepressant
Post-traumatic stress disorder
Obsessive compulsive disorder | | Drug interactions | Sertraline is not a potent inhibitor of CYP3A4, and because CYP2D6 metabolism is a minor pathway for
sertraline, drug–drug interactions with these isoforms is unlikely to be of clinical importance. Sertraline is
metabolized by more than one CYP isoform in parallel; therefore, drug interactions or genetic polymorphisms
are unlikely to cause clinically significant drug interaction via CYP isoform inhibition. Caution is advised,
however, when coadministering sertraline with potential object drugs, especially those with narrow
therapeutic indices in elderly patients. For example, sertraline has been shown to reduce the clearance of
desipramine and imipramine as a result of CYP2D6 inhibition.
Because sertraline is highly protein bound, patients receiving it concurrently with any highly protein-bound
drug should be observed for potential adverse effects associated with combined therapy. | | Metabolism | Sertraline undergoes extensive first-pass metabolism
in the liver. The main pathway is demethylation to
inactive N-desmethylsertraline, a process that appears
to involve multiple cytochrome P450 isoenzymes;
further metabolism and glucuronide conjugation occurs.
Sertraline is excreted in about equal amounts in the urine
and faeces, mainly as metabolites. |
| | Sertraline Preparation Products And Raw materials |
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