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==Pharmacology==
==Pharmacology==
===Binding profile===
===Binding profile===
Ziprasidone acts as an [[receptor antagonist|antagonist]]/[[inverse agonist]] of the following [[receptor (biochemistry)|receptor]]s:<ref name="AkiskalTohen2011">{{cite book | author1 = Hagop S. Akiskal | author2 = Mauricio Tohen | title = Bipolar Psychopharmacotherapy: Caring for the Patient | url = http://books.google.com/books?id=u0fO8RRIE1MC&pg=PT209 | accessdate = 13 May 2012 | date = 24 June 2011 | publisher = John Wiley & Sons | isbn = 978-1-119-95664-8 | page = 209}}</ref>
Ziprasidone acts as an [[receptor antagonist|antagonist]]/[[inverse agonist]] (unless otherwise noted) of the following [[receptor (biochemistry)|receptor]]s and [[membrane transport protein|transporter]]s:<ref name="AkiskalTohen2011">{{cite book | author1 = Hagop S. Akiskal | author2 = Mauricio Tohen | title = Bipolar Psychopharmacotherapy: Caring for the Patient | url = http://books.google.com/books?id=u0fO8RRIE1MC&pg=PT209 | accessdate = 13 May 2012 | date = 24 June 2011 | publisher = John Wiley & Sons | isbn = 978-1-119-95664-8 | page = 209}}</ref><ref name="pmid7562537">{{cite journal | author = Seeger TF, Seymour PA, Schmidt AW, ''et al.'' | title = Ziprasidone (CP-88,059): a new antipsychotic with combined dopamine and serotonin receptor antagonist activity | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 275 | issue = 1 | pages = 101–13 | year = 1995 | month = October | pmid = 7562537 | doi = | url = http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=7562537}}</ref><ref name="pmid8935801">{{cite journal | author = Schotte A, Janssen PF, Gommeren W, ''et al.'' | title = Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding | journal = Psychopharmacology | volume = 124 | issue = 1-2 | pages = 57–73 | year = 1996 | month = March | pmid = 8935801 | doi = | url = http://link.springer.de/link/service/journals/00213/bibs/61241-2/61240057.htm}}</ref><ref name="PDSP-DB">[http://pdsp.med.unc.edu/pdsp.php?knowID=&kiKey=&receptorDD=&receptor=&speciesDD=&species=&sourcesDD=&source=&hotLigandDD=&hotLigand=&testLigandDD=&testFreeRadio=testFreeRadio&testLigand=ziprasidone&referenceDD=&reference=&KiGreater=&KiLess=&kiAllRadio=all&doQuery=Submit+Query PDSP certified data]</ref>


<table><tr><td>
⚫
* [[D2 receptor|D<sub>2</sub> receptor]] (K<sub>i</sub> = 4.8 nM)
* [[5-HT1A receptor|5-HT<sub>1A</sub> receptor]] (K<sub>i</sub> = 3.4 nM) ([[partial agonist]])<ref name="pmid9760039">{{cite journal | author = Newman-Tancredi A, Gavaudan S, Conte C, ''et al.'' | title = Agonist and antagonist actions of antipsychotic agents at 5-HT1A receptors: a [35S]GTPgammaS binding study | journal = European Journal of Pharmacology | volume = 355 | issue = 2-3 | pages = 245–56 | year = 1998 | month = August | pmid = 9760039 | doi = | url = http://linkinghub.elsevier.com/retrieve/pii/S0014-2999(98)00483-X}}</ref>
⚫
* [[D3 receptor|D<sub>3</sub> receptor]] (K<sub>i</sub> = 7.2 nM)
* [[5-HT1B receptor|5-HT<sub>1B</sub> receptor]] (K<sub>i</sub> = 4.0 nM) (partial agonist)<ref name="SeifertWieland2006">{{cite book | author1 = Roland Seifert | author2 = Thomas Wieland | author3 = Raimund Mannhold | coauthors = Hugo Kubinyi, Gerd Folkers | title = G Protein-Coupled Receptors as Drug Targets: Analysis of Activation and Constitutive Activity | url = http://books.google.com/books?id=pIrnOKH-7HcC&pg=PA227 | accessdate = 13 May 2012 | date = 17 July 2006 | publisher = John Wiley & Sons | isbn = 978-3-527-60695-5 | page = 227}}</ref>
* [[5-HT1D receptor|5-HT<sub>1D</sub> receptor]] (K<sub>i</sub> = 2.3 nM)
* [[5-HT1D receptor|5-HT<sub>1D</sub> receptor]] (K<sub>i</sub> = 2.3 nM)
* [[5-HT1E receptor|5-HT<sub>1E</sub> receptor]] (K<sub>i</sub> = 360 nM)
* [[5-HT1F receptor|5-HT<sub>1F</sub> receptor]] (K<sub>i</sub> = >10,000 nM) (inactive)<ref name="pmid16918396">{{cite journal | author = Wood MD, Scott C, Clarke K, ''et al.'' | title = Pharmacological profile of antipsychotics at monoamine receptors: atypicality beyond 5-HT2A receptor blockade | journal = CNS & Neurological Disorders Drug Targets | volume = 5 | issue = 4 | pages = 445–52 | year = 2006 | month = August | pmid = 16918396 | doi = | url = http://www.benthamdirect.org/pages/content.php?CNSNDDT/2006/00000005/00000004/0009Z.SGM}}</ref>
* [[5-HT2A receptor|5-HT<sub>2A</sub> receptor]] (K<sub>i</sub> = 0.4 nM)
* [[5-HT2A receptor|5-HT<sub>2A</sub> receptor]] (K<sub>i</sub> = 0.4 nM)
* [[5-HT2B receptor|5-HT<sub>2B</sub> receptor]] (K<sub>i</sub> = 27 nM)
* [[5-HT2C receptor|5-HT<sub>2C</sub> receptor]] (K<sub>i</sub> = 1.3 nM)
* [[5-HT2C receptor|5-HT<sub>2C</sub> receptor]] (K<sub>i</sub> = 1.3 nM)
* [[alpha-1 adrenergic receptor|α<sub>1</sub>-adrenergic receptor]] (K<sub>i</sub> = 10 nM)
* [[5-HT3 receptor|5-HT<sub>3</sub> receptor]] (K<sub>i</sub> = > 10,000 nM) (inactive)
* [[H1 receptor|H<sub>1</sub> receptor]] (K<sub>i</sub> = 47 nM)
* [[5-HT5A receptor|5-HT<sub>5A</sub> receptor]] (K<sub>i</sub> = 291 nM)
* [[5-HT6 receptor|5-HT<sub>6</sub> receptor]] (K<sub>i</sub> = 61 nM)

* [[5-HT7 receptor|5-HT<sub>7</sub> receptor]] (K<sub>i</sub> = 6 nM)
And as an [[agonist]] of the following receptors:<ref name="AkiskalTohen2011" />
</td><td>

* [[5-HT1A receptor|5-HT<sub>1A</sub> receptor]] (K<sub>i</sub> = 3.4 nM) ([[partial agonist]])
* [[D1 receptor|D<sub>1</sub> receptor]] (K<sub>i</sub> = 525 nM)
⚫
* [[D2 receptor|D<sub>2</sub> receptor]] (K<sub>i</sub> = 4.8 nM)

⚫
* [[D3 receptor|D<sub>3</sub> receptor]] (K<sub>i</sub> = 7.2 nM)
It also has some activity as a [[transporter blocker|blocker]] of the [[serotonin transporter|SERT]] and [[norepinephrine transporter|NET]].<ref name="AkiskalTohen2011" />
* [[D4 receptor|D<sub>4</sub> receptor]] (K<sub>i</sub> = 32 nM)

Notably, ziprasidone has negligible affinity for the [[muscarinic acetylcholine receptor|mACh receptor]]s (IC<sub>50</sub> >1000 nM).<ref name="AkiskalTohen2011" />
* [[D5 receptor|D<sub>5</sub> receptor]] (K<sub>i</sub> = 152 nM)
* [[alpha-1 adrenergic receptor|α<sub>1</sub>-adrenergic receptor]] (K<sub>i</sub> = 11 nM)
* [[alpha-2 adrenergic receptor|α<sub>2</sub>-adrenergic receptor]] (K<sub>i</sub> = 260 nM)
* [[H1 receptor|H<sub>1</sub> receptor]] (K<sub>i</sub> = 50 nM)
* [[Muscarinic acetylcholine receptor|mACh receptor]]s (K<sub>i</sub> = >10,000 nM) (inactive)
* [[Serotonin transporter|5-HT transporter]] (K<sub>i</sub> = 53 nM) ([[reuptake inhibitor|inhibitor]])<ref name="pmid10192829">{{cite journal | author = Daniel DG, Zimbroff DL, Potkin SG, Reeves KR, Harrigan EP, Lakshminarayanan M | title = Ziprasidone 80 mg/day and 160 mg/day in the acute exacerbation of schizophrenia and schizoaffective disorder: a 6-week placebo-controlled trial. Ziprasidone Study Group | journal = Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology | volume = 20 | issue = 5 | pages = 491–505 | year = 1999 | month = May | pmid = 10192829 | doi = 10.1016/S0893-133X(98)00090-6 | url = http://dx.doi.org/10.1016/S0893-133X(98)00090-6}}</ref>
* [[Norepinephrine transporter|NE transporter]] (K<sub>i</sub> = 48 nM) (inhibitor)<ref name="pmid10192829" />
* [[Dopamine transporter|DA transporter]] (K<sub>i</sub> = >10,000 nM) (inactive)<ref name="PDSP-DB" />
</td></tr></table>


===Correspondance to clinical effects===
===Correspondance to clinical effects===
Ziprasidone's [[affinity (pharmacology)|affinities]] for the [[dopamine receptor|dopamine]], [[serotonin receptor|serotonin]], and [[alpha-1 adrenergic receptor|α<sub>1</sub>-adrenergic receptor]]s are high and its affinity for the [[H1 receptor|histamine H<sub>1</sub> receptor]] is moderate.<ref name="AkiskalTohen2011" /><ref name="pmid16381088">{{cite journal | author = Nemeroff CB, Lieberman JA, Weiden PJ, ''et al.'' | title = From clinical research to clinical practice: a 4-year review of ziprasidone | journal = CNS Spectrums | volume = 10 | issue = 11 Suppl 17 | pages = 1–20 | year = 2005 | month = November | pmid = 16381088 | doi = | url = http://www.cnsspectrums.com/aspx/articledetail.aspx?articleid=403}}</ref> It also displays some inhibition of synaptic reuptake of [[serotonin]] and [[norepinephrine]].<ref name="AkiskalTohen2011" /><ref name="pmid10193665">{{cite journal | author = Tatsumi M, Jansen K, Blakely RD, Richelson E | title = Pharmacological profile of neuroleptics at human monoamine transporters | journal = European Journal of Pharmacology | volume = 368 | issue = 2-3 | pages = 277–83 | year = 1999 | month = March | pmid = 10193665 | doi = | url = }}</ref>
Ziprasidone's [[affinity (pharmacology)|affinities]] for the [[dopamine receptor|dopamine]], [[serotonin receptor|serotonin]], and [[alpha-1 adrenergic receptor|α<sub>1</sub>-adrenergic receptor]]s are high and its affinity for the [[H1 receptor|histamine H<sub>1</sub> receptor]] is moderate.<ref name="AkiskalTohen2011" /><ref name="pmid16381088">{{cite journal | author = Nemeroff CB, Lieberman JA, Weiden PJ, ''et al.'' | title = From clinical research to clinical practice: a 4-year review of ziprasidone | journal = CNS Spectrums | volume = 10 | issue = 11 Suppl 17 | pages = 1–20 | year = 2005 | month = November | pmid = 16381088 | doi = | url = http://www.cnsspectrums.com/aspx/articledetail.aspx?articleid=403}}</ref> It also displays some inhibition of synaptic reuptake of [[serotonin]] and [[norepinephrine]].<ref name="AkiskalTohen2011" /><ref name="pmid10193665">{{cite journal | author = Tatsumi M, Jansen K, Blakely RD, Richelson E | title = Pharmacological profile of neuroleptics at human monoamine transporters | journal = European Journal of Pharmacology | volume = 368 | issue = 2-3 | pages = 277–83 | year = 1999 | month = March | pmid = 10193665 | doi = | url = }}</ref>


Ziprasidone's efficacy in treating the positive symptoms of schizophrenia is believed to be mediated primarily via antagonism of the dopamine receptors, specifically D<sub>2</sub>. Blockade of the 5-HT<sub>2A</sub> 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.<ref name="LüllmannMohr2006">{{cite book | author1 = Heinz Lüllmann | author2 = Klaus Mohr | title = Pharmakologie und Toxikologie: Arzneimittelwirkungen verstehen- Medikamente gezielt einsetzen; ein Lehrbuch für Studierende der Medizin, der Pharmazie und der Biowissenschaften, eine Informationsquelle für Ärzte, Apotheker und Gesundheitspolitiker | url = http://books.google.com/books?id=7ewS8QAClYEC&pg=PP1 | accessdate = 13 May 2012 | year = 2006 | publisher = Georg Thieme Verlag | isbn = 978-3-13-368516-0 | page = }}</ref> Blockade of 5-HT<sub>2A</sub> and 5-HT<sub>2C</sub> and activation of 5-HT<sub>1A</sub> as well as inhibition of the reuptake of serotonin and norepinephrine may all contribute to its ability to alleviate negative symptoms. The relatively weak antagonistic actions of ziprasidone on the α<sub>1</sub>-adrenergic and H<sub>1</sub> receptors likely in part explain some of its side effects, such as [[sedation]] and [[orthostatic hypotension]]. Unlike many other antipsychotics, ziprasidone has no significant affinity for the mACh receptors, and as such lacks any [[anticholinergic]] side effects.
Ziprasidone's efficacy in treating the positive symptoms of schizophrenia is believed to be mediated primarily via antagonism of the dopamine receptors, specifically D<sub>2</sub>. Blockade of the 5-HT<sub>2A</sub> 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.<ref name="LüllmannMohr2006">{{cite book | author1 = Heinz Lüllmann | author2 = Klaus Mohr | title = Pharmakologie und Toxikologie: Arzneimittelwirkungen verstehen- Medikamente gezielt einsetzen; ein Lehrbuch für Studierende der Medizin, der Pharmazie und der Biowissenschaften, eine Informationsquelle für Ärzte, Apotheker und Gesundheitspolitiker | url = http://books.google.com/books?id=7ewS8QAClYEC&pg=PP1 | accessdate = 13 May 2012 | year = 2006 | publisher = Georg Thieme Verlag | isbn = 978-3-13-368516-0 | page = }}</ref> Blockade of 5-HT<sub>2A</sub> and 5-HT<sub>2C</sub> and activation of 5-HT<sub>1A</sub> as well as inhibition of the reuptake of serotonin and norepinephrine may all contribute to its ability to alleviate negative symptoms.<ref name="SchatzbergNemeroff2006">{{cite book | author1 = Alan F. Schatzberg | author2 = Charles B. Nemeroff | title = Essentials of Clinical Psychopharmacology | url = http://books.google.com/books?id=i5zrVD1PAwEC&pg=PA297 | accessdate = 13 May 2012 | date = 10 February 2006 | publisher = American Psychiatric Pub | isbn = 978-1-58562-243-6 | page = 297}}</ref> The relatively weak antagonistic actions of ziprasidone on the α<sub>1</sub>-adrenergic and H<sub>1</sub> receptors likely in part explain some of its side effects, such as [[sedation]] and [[orthostatic hypotension]]. Unlike many other antipsychotics, ziprasidone has no significant affinity for the mACh receptors, and as such lacks any [[anticholinergic]] side effects.


==Pharmacokinetics==
==Pharmacokinetics==

Revision as of 21:28, 13 May 2012

Ziprasidone
Clinical data
Trade namesGeodon
AHFS/Drugs.comMonograph
MedlinePlusa699062
License data
Routes of
administration		Oral, IM
ATC code
Legal status
Legal status
  • US: WARNING[1]
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability60% (oral)
100% (IM)
Metabolismhepatic (aldehyde reductase)
Elimination half-life7 hours
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=C5Nc1c(cc(c(Cl)c1)CCN4CCN(c3nsc2ccccc23)CC4)C5
  • 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) was the fifth atypical antipsychotic to gain FDA approval (February 2001). In the United States, Ziprasidone is Food and Drug Administration (FDA) approved for the treatment of schizophrenia, and the intramuscular injection form of ziprasidone is approved for acute agitation in schizophrenic patients. Ziprasidone has also received approval for acute treatment of mania and mixed states associated with bipolar disorder. The brand name Geodon has been suggested to bring to mind the phrase 'down (don) to earth (geo)' referring to the goals of the medication.

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.

Geodon was one of five drugs which Pfizer pleaded guilty to misbranding "with the intent to defraud or mislead" in 2009 as a result of a qui tam lawsuit by Stefan P. Kruszewski. Pfizer agreed to pay $2.3 billion (£1.4 billion) in settlement, and entered a corporate integrity agreement. Pfizer was found to have illegally promoted four of its drugs for use in conditions that had not been approved by the FDA.[2]

Pharmacology

Binding profile

Ziprasidone acts as an antagonist/inverse agonist (unless otherwise noted) of the following receptors and transporters:[3][4][5][6]

Correspondance to clinical effects

Ziprasidone's affinities for the dopamine, serotonin, and α1-adrenergic receptors are high and its affinity for the histamine H1 receptor is moderate.[3][11] It also displays some inhibition of synaptic reuptake of serotonin and norepinephrine.[3][12]

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 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.[13] 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.[14] The relatively weak antagonistic actions of ziprasidone on the α1-adrenergic and H1 receptors likely in part explain some of its side effects, such as sedation and orthostatic hypotension. Unlike many other antipsychotics, ziprasidone has no significant affinity for the mACh receptors, and as such lacks any anticholinergic side effects.

Pharmacokinetics

The systemic bioavailability of ziprasidone administered intramuscularly is 100%, or 60%, administered orally with food. After a single dose intramuscular administration, the peak serum concentration typically occurs at about 60 minutes after the dose is administered, or earlier. Steady state plasma concentrations are achieved within one to three days. The mean half-life ranges from two to five hours. 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%.[15][16]

Ziprasidone is hepatically metabolized by aldehyde oxidase; minor metabolism occurs via cytochrome P450 3A4 (CYP3A4).[17] Medications that induce (e.g. carbamazepine) or inhibit (e.g. ketoconazole) CYP3A4 have been shown to decrease and increase, respectively, blood levels of ziprasidone.[18][19]

Adverse effects

Ziprasidone received a black box warning due to increased mortality in elderly patients with dementia-related psychosis.[15] It also slightly increases the QTc interval in some patients and increases the risk of a potentially lethal type of heart arrhythmia known as torsades de pointes. Ziprasidone should be used cautiously in patients taking other medications likely to interact with ziprasidone or increase the QTc interval.[20]

Ziprasidone is known to cause activation into mania in some bipolar patients.[21][22][23]

This medication can cause birth defects, according to animal studies, although this side effect has not been confirmed in humans.[15]

Adverse events reported for ziprasidone include severe chest pains, impaired erectile function and stimulation, sedation, insomnia, orthostasis, life-threatening neuroleptic malignant syndrome, akathisia, and the development of permanent neurological disorder tardive dyskinesia. Rarely, temporary speech disorders may result.

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 may not be as bad as some of the other atypical antipsychotics (namely, olanzapine (Zyprexa)) at causing insulin resistance and weight gain.[24][25][26][27] In fact, in a trial of long term therapy with ziprasidone, overweight patients (BMI > 27) actually had a mean weight loss overall.[15] However, Ziprasidone is not a weight loss drug. The weight loss reflected in this study on ziprasidone was really reflective of patients who had gained weight on other antipsychotics who were now trending back toward their baseline. [citation needed] According to the manufacturer insert , ziprasidone caused an average weight gain of 2.2 kg (4.8 lbs) (which is significantly lower than other atypicals–clozapine and olanzapine).

Discontinuation

Ziprasidone should be discontinued gradually, with careful consideration from the prescribing doctor, to avoid withdrawal symptoms or relapse. Withdrawal may become even more difficult after failed attempts.[citation needed]

The British National Formulary recommends a gradual withdrawal when discontinuing anti-psychotic treatment to avoid acute withdrawal syndrome or rapid relapse.[28] Due to compensatory changes at dopamine, serotonin, adrenergic and histamine receptor sites in the central nervous system, withdrawal symptoms can occur during abrupt or over-rapid reduction in dosage. However, despite increasing demand for safe and effective antipsychotic withdrawal protocols or dose-reduction schedules, no specific guidelines with proven safety and efficacy are currently available. Some have suggested using the Ashton Manual http://www.benzo.org.uk/manual/, originally developed for benzodiazapine withdrawal. Support groups such as The Icarus Project http://theicarusproject.net/HarmReductionGuideComingOffPsychDrugs, and other online forums provide resources and social support for those attempting to discontinue antipsychotics and other psychiatric medications. Withdrawal symptoms reported to occur after discontinuation of antipsychotics include nausea, emesis, lightheadedness, diaphoresis, dyskinesia, orthostasis, tachycardia, nervousness, dizziness, headache, excessive non-stop crying, and anxiety.[29][30] Some have argued that additional somatic and psychiatric symptoms associated with dopaminergic super-sensitivity, including dyskinesia and acute psychosis, are common features of withdrawal in individuals treated with neuroleptics.[31][32][33][34] This has led some to suggest that the withdrawal process might itself be schizo-mimetic, producing schizophrenia-like symptoms even in previously healthy patients, indicating a possible pharmacological origin of mental illness in a yet unknown percentage of patients currently and previously treated with antipsychotics. This question is unresolved, and remains a highly controversial issue among professionals in the medical and mental health communities, as well the public.[35] Complicated and long-lasting rebound insomnia symptoms can also occur after withdrawing from antipsychotics.[36]

Overdose

Ziprasidone doses as large as 3,240 mg have been "survived without sequelae." The most common effects reported by Pfizer include extrapyramidal reactions, somnolence, tremor, and anxiety.

References

  1. ^ "FDA-sourced list of all drugs with black box warnings (Use Download Full Results and View Query links.)". nctr-crs.fda.gov. FDA. Retrieved 22 Oct 2023.
  2. ^ "Pfizer agrees record fraud fine". BBC News. British Broadcasting Corporation. 2 September 2009.
  3. ^ a b c Hagop S. Akiskal; Mauricio Tohen (24 June 2011). Bipolar Psychopharmacotherapy: Caring for the Patient. John Wiley & Sons. p. 209. ISBN 978-1-119-95664-8. Retrieved 13 May 2012.
  4. ^ Seeger TF, Seymour PA, Schmidt AW; et al. (1995). "Ziprasidone (CP-88,059): a new antipsychotic with combined dopamine and serotonin receptor antagonist activity". The Journal of Pharmacology and Experimental Therapeutics. 275 (1): 101–13. PMID 7562537. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  5. ^ Schotte A, Janssen PF, Gommeren W; et al. (1996). "Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding". Psychopharmacology. 124 (1–2): 57–73. PMID 8935801. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  6. ^ a b PDSP certified data
  7. ^ Newman-Tancredi A, Gavaudan S, Conte C; et al. (1998). "Agonist and antagonist actions of antipsychotic agents at 5-HT1A receptors: a [35S]GTPgammaS binding study". European Journal of Pharmacology. 355 (2–3): 245–56. PMID 9760039. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  8. ^ Roland Seifert; Thomas Wieland; Raimund Mannhold (17 July 2006). G Protein-Coupled Receptors as Drug Targets: Analysis of Activation and Constitutive Activity. John Wiley & Sons. p. 227. ISBN 978-3-527-60695-5. Retrieved 13 May 2012. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  9. ^ Wood MD, Scott C, Clarke K; et al. (2006). "Pharmacological profile of antipsychotics at monoamine receptors: atypicality beyond 5-HT2A receptor blockade". CNS & Neurological Disorders Drug Targets. 5 (4): 445–52. PMID 16918396. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  10. ^ a b Daniel DG, Zimbroff DL, Potkin SG, Reeves KR, Harrigan EP, Lakshminarayanan M (1999). "Ziprasidone 80 mg/day and 160 mg/day in the acute exacerbation of schizophrenia and schizoaffective disorder: a 6-week placebo-controlled trial. Ziprasidone Study Group". Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology. 20 (5): 491–505. doi:10.1016/S0893-133X(98)00090-6. PMID 10192829. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  11. ^ Nemeroff CB, Lieberman JA, Weiden PJ; et al. (2005). "From clinical research to clinical practice: a 4-year review of ziprasidone". CNS Spectrums. 10 (11 Suppl 17): 1–20. PMID 16381088. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  12. ^ Tatsumi M, Jansen K, Blakely RD, Richelson E (1999). "Pharmacological profile of neuroleptics at human monoamine transporters". European Journal of Pharmacology. 368 (2–3): 277–83. PMID 10193665. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  13. ^ Heinz Lüllmann; Klaus Mohr (2006). Pharmakologie und Toxikologie: Arzneimittelwirkungen verstehen- Medikamente gezielt einsetzen; ein Lehrbuch für Studierende der Medizin, der Pharmazie und der Biowissenschaften, eine Informationsquelle für Ärzte, Apotheker und Gesundheitspolitiker. Georg Thieme Verlag. ISBN 978-3-13-368516-0. Retrieved 13 May 2012.
  14. ^ Alan F. Schatzberg; Charles B. Nemeroff (10 February 2006). Essentials of Clinical Psychopharmacology. American Psychiatric Pub. p. 297. ISBN 978-1-58562-243-6. Retrieved 13 May 2012.
  15. ^ a b c d "Geodon Prescribing Information" (PDF). Pfizer, Inc. Retrieved 2009-01-26.
  16. ^ Miceli JJ, Glue P, Alderman J, Wilner K (2007). "The effect of food on the absorption of oral ziprasidone". Psychopharmacology Bulletin. 40 (3): 58–68. PMID 18007569.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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  36. ^ Geodon Withdrawal Retrieved on 3 August 2011

Further reading

External links


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