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| metabolism = Hepatic ([[aldehyde reductase]])
| metabolism = Hepatic ([[aldehyde reductase]])
| elimination_half-life = 7 to 10 hours<ref name=2007rev>{{cite journal|title=Ziprasidone in the treatment of mania in bipolar disorder.|journal=Neuropsychiatr Dis Treat|date=December 2007|volume=3|issue=6|pages=823-34|pmid=19300617|pmc=2656324}}</ref>
| elimination_half-life = 7<ref name="la-press.com"/>- 10 hours<ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656324/</ref>


| excretion = Urine and feces
| excretion = Urine and feces
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Ziprasidone is hepatically metabolized by [[aldehyde oxidase]]; minor metabolism occurs via [[CYP3A4|cytochrome P450 3A4]] (CYP3A4).<ref name=Sandson>{{cite journal |vauthors=Sandson NB, Armstrong SC, Cozza KL |title=An overview of psychotropic drug-drug interactions |journal=Psychosomatics |volume=46 |issue=5 |pages=464–94 |year=2005 |pmid=16145193 |doi=10.1176/appi.psy.46.5.464}}</ref> Medications that induce (e.g. [[carbamazepine]]) or inhibit (e.g. [[ketoconazole]]) CYP3A4 have been shown to decrease and increase, respectively, blood levels of ziprasidone.<ref name="pmid10771457">{{cite journal |vauthors=Miceli JJ, Anziano RJ, Robarge L, Hansen RA, Laurent A | title = The effect of carbamazepine on the steady-state pharmacokinetics of ziprasidone in healthy volunteers | journal = British Journal of Clinical Pharmacology | volume = 49 Suppl 1 | issue = | pages = 65S–70S | year = 2000 | pmid = 10771457 | pmc = 2015057 | doi = 10.1046/j.1365-2125.2000.00157.x| url = http://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0306-5251&date=2000&volume=49&issue=&spage=65S}}</ref><ref name="pmid10771458">{{cite journal |vauthors=Miceli JJ, Smith M, Robarge L, Morse T, Laurent A | title = The effects of ketoconazole on ziprasidone pharmacokinetics—a placebo-controlled crossover study in healthy volunteers | journal = British Journal of Clinical Pharmacology | volume = 49 Suppl 1 | issue = | pages = 71S–76S | year = 2000 | pmid = 10771458 | pmc = 2015056 | doi = 10.1046/j.1365-2125.2000.00156.x| url = http://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0306-5251&date=2000&volume=49&issue=&spage=71S}}</ref>
Ziprasidone is hepatically metabolized by [[aldehyde oxidase]]; minor metabolism occurs via [[CYP3A4|cytochrome P450 3A4]] (CYP3A4).<ref name=Sandson>{{cite journal |vauthors=Sandson NB, Armstrong SC, Cozza KL |title=An overview of psychotropic drug-drug interactions |journal=Psychosomatics |volume=46 |issue=5 |pages=464–94 |year=2005 |pmid=16145193 |doi=10.1176/appi.psy.46.5.464}}</ref> Medications that induce (e.g. [[carbamazepine]]) or inhibit (e.g. [[ketoconazole]]) CYP3A4 have been shown to decrease and increase, respectively, blood levels of ziprasidone.<ref name="pmid10771457">{{cite journal |vauthors=Miceli JJ, Anziano RJ, Robarge L, Hansen RA, Laurent A | title = The effect of carbamazepine on the steady-state pharmacokinetics of ziprasidone in healthy volunteers | journal = British Journal of Clinical Pharmacology | volume = 49 Suppl 1 | issue = | pages = 65S–70S | year = 2000 | pmid = 10771457 | pmc = 2015057 | doi = 10.1046/j.1365-2125.2000.00157.x| url = http://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0306-5251&date=2000&volume=49&issue=&spage=65S}}</ref><ref name="pmid10771458">{{cite journal |vauthors=Miceli JJ, Smith M, Robarge L, Morse T, Laurent A | title = The effects of ketoconazole on ziprasidone pharmacokinetics—a placebo-controlled crossover study in healthy volunteers | journal = British Journal of Clinical Pharmacology | volume = 49 Suppl 1 | issue = | pages = 71S–76S | year = 2000 | pmid = 10771458 | pmc = 2015056 | doi = 10.1046/j.1365-2125.2000.00156.x| url = http://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0306-5251&date=2000&volume=49&issue=&spage=71S}}</ref>


It's biological half-life time is 10 hours at doses 80-120 milligrams.<ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656324/</ref>
It's biological half-life time is 10 hours at doses 80-120 milligrams.<ref name=2007rev/>


==Society and culture==
==Society and culture==

Revision as of 19:05, 6 November 2016

Ziprasidone
Clinical data
Trade namesGeodon, Zeldox, Zipwell
AHFS/Drugs.comMonograph
MedlinePlusa699062
License data
Pregnancy
category
  • AU: B3
Routes of
administration		Oral (capsules), IM
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability60% (oral[2])
100% (IM)
MetabolismHepatic (aldehyde reductase)
Elimination half-life7 to 10 hours[3]
ExcretionUrine and feces
Identifiers
  • 5-{2-[4-(1,2-benzisothiazol-3-yl)-1-piperazinyl]ethyl}-6-chloro-1,3-dihydro-2H-indol-2-one
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.106.954 Edit this at Wikidata
Chemical and physical data
FormulaC21H21ClN4OS
Molar mass412.936 g/mol g·mol−1
3D model (JSmol)
  • O=C1Cc2c(N1)cc(Cl)c(c2)CCN3CCN(CC3)c4nsc5ccccc45
  • InChI=1S/C21H21ClN4OS/c22-17-13-18-15(12-20(27)23-18)11-14(17)5-6-25-7-9-26(10-8-25)21-16-3-1-2-4-19(16)28-24-21/h1-4,11,13H,5-10,12H2,(H,23,27) checkY
  • Key:MVWVFYHBGMAFLY-UHFFFAOYSA-N checkY
  (verify)

Ziprasidone (marketed as Geodon, Zeldox by Pfizer and Zipwell by Actavis) was the fifth atypical antipsychotic to gain approval (February 5, 2001[4]) in the United States. It is approved by the U.S. Food and Drug Administration (FDA) for the treatment of schizophrenia, and acute mania and mixed states associated with bipolar disorder.[5] Its intramuscular injection form is approved for acute agitation in schizophrenic patients for whom treatment with just ziprasidone is appropriate. Ziprasidone is also used off-label for depression, bipolar maintenance, and PTSD.[6]

The oral form of ziprasidone is the hydrochloride salt, ziprasidone hydrochloride. The intramuscular form, on the other hand, is the mesylate salt, ziprasidone mesylate trihydrate, and is provided as a lyophilized powder.

Medical uses

Ziprazidone is approved by the U.S. Food and Drug Administration (FDA) for the treatment of schizophrenia, and acute mania and mixed states associated with bipolar disorder. Its intramuscular injection form is approved for acute agitation in schizophrenic patients for whom treatment with just ziprasidone is appropriate.[7]

Ziprasidone is effective in the treatment of schizophrenia, though evidence from the CATIE trials suggests it is less effective than olanzapine and of around equal effectiveness to quetiapine. There are higher discontinuation rates for lower doses of Ziprasidone, which are also less effective than higher doses.[8]

Discontinuation

The British National Formulary recommends a gradual withdrawal when discontinuing antipsychotic treatment to avoid acute withdrawal syndrome or rapid relapse.[9]

Adverse effects

Ziprasidone received a black box warning due to increased mortality in elderly patients with dementia-related psychosis.[10]

Sleepiness and headache are very common adverse effects (>10%).[11][12]

Common adverse effects (1–10%), include producing too much saliva or having dry mouth, runny nose, respiratory disorders or coughing, nausea and vomiting, stomach aches, constipation or diarrhea, loss of appetite, weight gain (but the smallest risk for weight gain compared to other antipsychotics[13]), rashes, fast heart beats, blood pressure falling when standing up quickly, muscle pain, weakness, twitches, dizziness, and anxiety.[11][12] Extrapyramidal symptoms are also common and include tremor, dystonia (sustained or repetitive muscle contractions), akathisia (the feeling of a need to be in motion), parkinsonism, and muscle rigidity; in a 2013 meta-analysis of 15 antipsychotic drugs, ziprasidone ranked 8th for such side effects.[14]

Ziprasidone is known to cause activation into mania in some bipolar patients.[15][16][17]

This medication can cause birth defects, according to animal studies, although this side effect has not been confirmed in humans.[10]

Recently, the FDA required the manufacturers of some atypical antipsychotics to include a warning about the risk of hyperglycemia and Type II diabetes with atypical antipsychotics. Some evidence suggests that ziprasidone does not cause insulin resistance to the degree of other atypical antipsychotics, such as Zyprexa. Weight gain is also less of a concern with Ziprasidone compared to other atypical antipsychotics)[18][19][20][21] In fact, in a trial of long term therapy with ziprasidone, overweight patients (BMI > 27) actually had a mean weight loss overall;[10] According to the manufacturer insert, ziprasidone caused an average weight gain of 2.2 kg (4.8 lbs), which is significantly lower than other atypical antipsychotics, making this medication better for patients that are concerned about their weight. In December 2014, the FDA warned that ziprasidone could cause a potentially fatal skin reaction, Drug Reaction with Eosinophilia and Systemic Symptoms, although this was believed to occur only rarely.[22]

Pharmacology

When the 5-HT2C-receptor is activated, a blockade of dopamine and serotonin occurs as well as the inhibition of norepinephrine release. Ziprasidone works by strongly blocking the 5-HT2C-receptor, increasing serotonin, norepinephrine and dopamine. The blocking of the 5-HT2C-receptor releases norepinephrine (norepinephrine increase implies increased blood sugar[23]), but the neuronal reuptake of norepinephrine is limited heavily by Ziprasidone from another part of it's mechanism.[24] Ziprasidone has no relationship to the 5-HT3-receptor (inactivated).

5-HT2A activation can upregulate D2 receptors. Ziprasidone blocks the 5-HT2A-receptor. The blockade of 5-HT2A-receptor also releases dopamine, just like a blockade of 5-HT2C. Ziprasidone is most potent at the 5-HT2A-receptor, next-most potent at 5-HT2C, and almost as much potent for the 5-HT1A-receptor.[13] However, at the 5-HT1A-receptor a partial agonism occurs, providing a theory as to the correlation between Ziprasidone and lack of weight gain.[25][26] The 5-HT6-receptor and 5-HT7-receptors may also be of some importance.[27]

It has bovine binding affinity for the 5-HT1D-receptor.[13][28][29][30] Ziprasidone has an unusually high affinity for 5-HT2A-receptor. The affinity for this 5HT-receptor is 11 times higher than the dopamine D2.[24] The affinity for the 5-HT2C-receptor is 10 times higher than for the dopamine D2.[2] Thus, a high affinity for the 5-HT2A-receptor will downregulate the D2-receptor. It blocks the dopamine D1 and the D3.[31] Ziprasidone inhibits neuronal reuptake of norepinephrine and effects the H1D-receptor,[32] which medications that do that stabilize mood in humans.[32][33] Data from Pfizer suggest that 5-HT1A-receptor agonist function is unusually high with the drug Ziprasidone compared to other antipsychotics[34] (agonism action at this 5HT-receptor improves cognition[35]). At the same time even touch of the 5-HT6-receptor,[36] why improved cognition is seen with Ziprasidone patients switched from other drugs.[36] Ziprasidone's block of histamine H1-receptors can explain the somnolence seen with patients. [37] The affinity rate for these H1-receptors is up to moderate.[37]

Binding profile

Ziprasidone acts as an antagonist/inverse agonist (unless otherwise noted) of the following receptors and transporters:[38][39][40][41][42]

Correspondence to clinical effects

Ziprasidone's affinities for most of the dopamine and serotonin receptors and the α1-adrenergic receptor are high and its affinity for the histamine H1 receptor is moderate.[38][46] It also displays some inhibition of synaptic reuptake of serotonin and norepinephrine, though not dopamine.[38][47]

Ziprasidone's efficacy in treating the positive symptoms of schizophrenia is believed to be mediated primarily via antagonism of the dopamine receptors, specifically D2. Blockade of the 5-HT2A receptor may also play a role in its effectiveness against positive symptoms, though the significance of this property in antipsychotic drugs is still debated among researchers.[48] Blockade of 5-HT2A and 5-HT2C and activation of 5-HT1A as well as inhibition of the reuptake of serotonin and norepinephrine may all contribute to its ability to alleviate negative symptoms.[49] The relatively weak antagonistic actions of ziprasidone on the α1-adrenergic receptor likely in part explains some of its side effects, such as orthostatic hypotension. Unlike many other antipsychotics, ziprasidone has no significant affinity for the mACh receptors, and as such lacks any anticholinergic side effects. Like most other antipsychotics, ziprasidone is sedating due primarily to serotonin and dopamine blockade.[50][51]

Pharmacokinetics

The systemic bioavailability of ziprasidone is 100% when administered intramuscularly and 60% when administered orally without food.[2]

After a single dose intramuscular administration, the peak serum concentration typically occurs at about 60 minutes after the dose is administered, or earlier.[52] Steady state plasma concentrations are achieved within one to three days. Exposure increases in a dose-related manner and following three days of intramuscular dosing, little accumulation is observed.

Ziprasidone absorption is optimally achieved when administered with food. Without a meal preceding dose, the bioavailability of the drug is reduced by approximately 50%.[10][53]

Ziprasidone is hepatically metabolized by aldehyde oxidase; minor metabolism occurs via cytochrome P450 3A4 (CYP3A4).[54] Medications that induce (e.g. carbamazepine) or inhibit (e.g. ketoconazole) CYP3A4 have been shown to decrease and increase, respectively, blood levels of ziprasidone.[55][56]

It's biological half-life time is 10 hours at doses 80-120 milligrams.[3]

Society and culture

Lawsuit

In September 2009, the U.S. Justice Department announced that Pfizer had been ordered to pay an historic fine of $2.3 billion as a penalty for fraudulent marketing of several drugs, including Geodon.[57] Pfizer had illegally promoted Geodon and caused false claims to be submitted to government health care programs for uses that were not medically accepted indications. The civil settlement also resolves allegations that Pfizer paid kickbacks to health care providers to induce them to prescribe Geodon, as well as other, drugs. This was the largest civil fraud settlement in history against a pharmaceutical company.

History

Ziprasidone was first synthesized on the Pfizer central research campus in Groton,Connecticut.[58] Phase I trials started in 1995.[59] In 1998 ziprasidone was approved in Sweden.[60][61] After the FDA raised concerns about long QT syndrome,more clinical trials were conducted and submitted to the FDA, which approved the drug in 2001.[59][62][63]

References

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Further reading

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