플루옥세틴

그림문자(GHS)

• 그림문자(GHS)

  

• 신호 어

  Warning

• 유해·위험 문구

  H302：삼키면 유해함

  H315：피부에 자극을 일으킴

  H319：눈에 심한 자극을 일으킴

  H335：호흡 자극성을 일으킬 수 있음

• 예방조치문구

  P261：분진·흄·가스·미스트·증기·...·스프레이의 흡입을 피하시오.

  P264：취급 후에는 손을 철저히 씻으시오.

  P264：취급 후에는 손을 철저히 씻으시오.

  P270：이 제품을 사용할 때에는 먹거나, 마시거나 흡연하지 마시오.

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  P280：보호장갑/보호의/보안경/안면보호구를 착용하시오.

  P301+P312：삼켜서 불편함을 느끼면 의료기관(의사)의 진찰을 받으시오.

  P302+P352：피부에 묻으면 다량의 물로 씻으시오.

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  P305+P351+P338：눈에 묻으면 몇 분간 물로 조심해서 씻으시오. 가능하면 콘택트렌즈를 제거하시오. 계속 씻으시오.

  P330：입을 씻어내시오.

  P332+P313：피부 자극이 생기면 의학적인 조치· 조언을 구하시오.

  P337+P313：눈에 대한 자극이 지속되면 의학적인 조치· 조언를 구하시오.

  P362：오염된 의복을 벗고 세척 후에 재사용하기

  P403+P233：용기는 환기가 잘 되는 곳에 단단히 밀폐하여 저장하시오.

  P405：밀봉하여 저장하시오.

  P501：...에 내용물 / 용기를 폐기 하시오.

플루옥세틴 MSDS

• (+/-)-N-Methyl-gamma-(4-(trifluoromethyl)phenoxy)benzenepropanamine

플루옥세틴 화학적 특성, 용도, 생산

• 용도

  antibacterial

• Biological Functions

  Fluoxetine (Prozac) is given in the morning because of its potential for being activating and causing insomnia. Food does not affect its systemic bioavailability and may actually lessen the nausea reported by some patients. Fluoxetine is highly bound to serum proteins and may interact with other highly protein bound drugs. It is demethylated in the liver to form an active metabolite, norfluoxetine. Inactive metabolites are excreted by the kidney.Doses must be reduced in patients with liver disease.
  The slow elimination of fluoxetine and norfluoxetine lead to special clinical concerns when adjusting doses and discontinuing this medication. Steady state is not reached until 4 to 6 weeks, and similarly, complete elimination takes 4 to 6 weeks after discontinuation of the medication. A 4- to 6-week waiting period should be permitted before starting a medication with potential for an interaction with fluoxetine, such as a monoamine oxidase inhibitor (MAOI). Additionally, fluoxetine is a potent inhibitor of cytochrome P450 2D6 and can significantly elevate levels of drugs metabolized by this route. Thus, coadministration of drugs with a narrow therapeutic index, such as TCAs and type 1C antiarrhythmics, including flecainide and propafenone, are a particular concern.

• 일반 설명

  In fluoxetine (Prozac), protonated in vivo, the protonatedamino group can H-bond to the ether oxygen electrons, whichcan generate the β-arylamino–like group, with the other arylserving as the characteristic “extra” aryl. The S-isomer ismuch more selective for SERT than for NET. The majormetabolite is the N-demethyl compound, which is as potent asthe parent and more selective (SERT versus NET).
  Therapy for 2 or more weeks is required for the antidepressanteffect. Somatodendritic 5-HT_1A autoreceptor desensitizationwith chronic exposure to high levels of 5-HT isthe accepted explanation for the delayed effect for this andother serotonin reuptake inhibitors.

• Mechanism of action

  Fluoxetine is a potent and selective inhibitor of 5-HT reuptake, but not of NE or dopamine uptake in the CNS. Its mechanism of action is common to the SSRIs. Fluoxetine does not interact directly with postsynaptic 5-HT receptors and has weak affinity for the other neuroreceptors. Both enantiomers of fluoxetine display similar affinities for human SERT. The NE:5-HT selectivity ratio, however, indicates that the S-enantiomer is approximately 100 times more selective for SERT inhibition than the R-enantiomer. The R-(+)-stereoisomer is approximately eight times more potent an inhibitor of SERT together with a longer duration of action than the S-(–)-isomer. However, the S-(–)-norfluoxetine metabolite is seven times more potent as an inhibitor of the 5-HT transporter than the R-(+)-metabolite, with a selectivity ratio approximately equivalent to that of S-fluoxetine.

• Pharmacokinetics

  The pharmacokinetics of fluoxetine fit the general characteristics of the SSRIs. Of particular importance is its long half-life contributing to its nonlinear pharmacokinetics. In vitro studies show that fluoxetine and norfluoxetine are potent inhibitors of CYP2D6 and CYP3A4 and less potent inhibitors of CYP2C9, CYP2C19 and CYP1A2. Fluoxetine is metabolized primarily by CYP2D6 N-demethylation to its active metabolite norfluoxetine and, to a lesser extent, O-dealkylation to form the inactive metabolite p-trifluoromethylphenol. Following oral administration, fluoxetine and its metabolites are excreted principally in urine, with approximately 73% as unidentified metabolites, 10% as norfluoxetine, 10% as norfluoxetine glucuronide, 5% as fluoxetine N-glucuronide, and 2% as unmetabolized drug.
  Both R- and S-Norfluoxetine were less potent than the corresponding enantiomers of fluoxetine as inhibitors of NE uptake. Inhibition of 5-HT uptake in cerebral cortex persisted for more than 24 hours after administration of S-norfluoxetine similarly to fluoxetine. Thus, S-norfluoxetine is the active N-demethylated metabolite responsible for the persistently potent and selective inhibition of 5-HT uptake in vivo.
  The pharmacokinetics of fluoxetine in healthy geriatric individuals do not differ substantially from those in younger adults. Because of its relatively long half-life and nonlinear pharmacokinetics, the possibility of altered pharmacokinetics in geriatric individuals could exist, particularly those with systemic disease and/or in those receiving multiple medications concurrently. The elimination half-lives of fluoxetine and norfluoxetine do not appear to be altered substantially in patients with renal or hepatic impairment.

• Pharmacology

  Fluoxetine is a phenylpropylamine that inhibits the neuronal reuptake of serotonin, which presumably has a direct relationship on antidepressant activity. This compound has either no effect or a small effect on the neuronal reuptake of norepinephrine and dopamine. In addition, it does not bind to cholinergic, histaminergic, or α-adrenergic receptors, which is believed to be the cause of tricyclic antidepressant side effects.

• Clinical Use

  Fluoxetine is a 3-phenoxy-3-phenylpropylamine that exhibits selectivity and high affinity for human SERT and low affinity for NET. It is marketed as a racemic mixture of R- and S-fluoxetine. Its selectivity for SERT inhibition depends on the position of the substituent in the phenoxy ring.

• Drug interactions

  Fluoxetine and its norfluoxetine metabolite, like many other drugs metabolized by CYP2D6, inhibit the activity of CYP2D6 and, potentially, may increase plasma concentrations of concurrently administered drugs that also are metabolized by this enzyme. Fluoxetine may make normal CYP2D6 metabolizers resemble poor metabolizers. Fluoxetine can inhibit its own CYP2D6 metabolism, resulting in higher-than-expected plasma concentrations during upward dose adjustments. Therefore, switching from fluoxetine to another SSRI or other serotonergic antidepressant requires a washout period of at least 5 weeks or a lowerthan-recommended initial dose with monitoring for adverse events.
  Fluoxetine is highly protein bound and may affect the free plasma concentration and, thus, the pharmacological effect of other highly protein-bound drugs (e.g., warfarin sodium).

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