yingweiwo

Ziprasidone free base

Alias: CP 88059; CP88059; CP-88,059-01; CP88059 hydrochloride; CP-88059; CP-88,059; Ziprasidone HCl; Geodon; Zeldox; Zipwell
Cat No.:V21556 Purity: ≥98%
Ziprasidone (CP-88,059; CP 88059; CP-88,059-01; Geodon; Zeldox; Zipwell) is a dopamine and serotonin (5-HT) receptor antagonist with antipsychotic effects.
Ziprasidone free base
Ziprasidone free base Chemical Structure CAS No.: 146939-27-7
Product category: 5-HT Receptor
This product is for research use only, not for human use. We do not sell to patients.
Size Price Stock Qty
100mg
250mg
500mg
1g
2g
Other Sizes

Other Forms of Ziprasidone free base:

  • Ziprasidone D8
  • Ziprasidone HCl hydrate
  • Ziprasidone HCl (CP-88059)
  • Ziprasidone mesylate trihydrate
  • Ziprasidone mesylate
Official Supplier of:
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Alternate Text
Top Publications Citing lnvivochem Products
Product Description

Ziprasidone (CP-88,059; CP 88059; CP-88,059-01; Geodon; Zeldox; Zipwell) is a dopamine and serotonin (5-HT) receptor antagonist with antipsychotic effects. It is authorized for the treatment of acute mania, mixed states linked to bipolar disorder, and schizophrenia and bipolar illness. When treating schizophrenia patients who respond best to treatment consisting solely of ziprasidone, its intramuscular injection form is authorized for use in cases of acute agitation. According to theories about ziprasidone's mode of action, serotonin type 2 (5HT2) and dopamine type 2 (D2) antagonistic interactions together mediate the drug's effectiveness in treating schizophrenia. The exact mechanism by which ziprasidone treats bipolar disorder is unknown, as it is with other medications that are effective in treating the condition.

Biological Activity I Assay Protocols (From Reference)
Targets
Rat 5-HT1A Receptor ( Ki = 3.4 nM ); human 5-HT1A Receptor ( Ki = 2.5 nM ); Rat D2 Receptor ( Ki = 4.8 nM ); Rat 5-HT2A ( Ki = 0.42 nM )
ln Vitro

In vitro activity: Ziprasidone (0-500 nM, 150 seconds) inhibits hERG current of the wild type[2].

ln Vivo
Ziprasidone (oral gavage; 20 mg/kg; once daily; 7 weeks) causes reduced levels of physical activity, weight loss, high resting energy expenditure, and an increased ability to produce heat when exposed to cold[3].
Cell Assay
Cell Line: HEK-293 cells
Concentration: 0-500 nM
Incubation Time: 150 seconds
Result: Blocked wild-type hERG current in a voltage- and concentration-dependent manner (IC50 = 120 nm).
Animal Protocol
Eight-week-old female Sprague-Dawley rats weighing 200 to 250 g
20 mg/kg
Oral gavage; 20 mg/kg; once daily; 7 weeks
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
In the absence of food, ziprasidone's oral bioavailability is 60%, and absorption may reach 100% if ziprasidone is taken with a meal containing at least 500 kcal. The difference in bioavailability has little to do with the fat content of the food and appears to be related to the bulk of the meal since more absorption occurs the longer ziprasidone remains in the stomach.
Ziprasidone is extensively metabolized after oral administration with only a small amount excreted in the urine (<1%) or feces (<4%) as unchanged drug.
The mean apparent volume of distribution of Ziprasidone is 1.5 L/kg.
The mean apparent systemic clearance is 7.5 mL/min/kg.
Ziprasidone is well absorbed after oral administration, reaching peak plasma concentrations in 6 to 8 hours. The absolute bioavailability of a 20 mg dose under fed conditions is approximately 60%. The absorption of ziprasidone is increased up to two-fold in the presence of food.
The bioavailability of ziprasidone administered intramuscularly is 100%. After intramuscular administration of single doses, peak serum concentrations typically occur at approximately 60 minutes post-dose or earlier ...
Steady-state concentrations are achieved within one to three days of dosing. The mean apparent systemic clearance is 7.5 mL/min/kg.
Ziprasidone has a mean apparent volume of distribution of 1.5 L/kg. It is greater than 99% bound to plasma proteins, binding primarily to albumin and alpha1-acid glycoprotein.
For more Absorption, Distribution and Excretion (Complete) data for Ziprasidone (11 total), please visit the HSDB record page.
Metabolism / Metabolites
Ziprasidone is heavily metabolized in the liver with less than 5% of the drug excreted unchanged in the urine. The primary reductive pathway is catalyzed by aldehyde oxidase, while 2 other less prominent oxidative pathways are catalyzed by CYP3A4. Ziprasidone is unlikely to interact with other medications metabolized by CYP3A4 since only 1/3 of the antipsychotic is metabolized by the CYP3A4 system. There are 12 identified ziprasidone metabolites (abbreviations italicized): Ziprasidone sulfoxide, ziprasidone sulfone, (6-chloro-2-oxo-2,3-dihydro-1H-indol-5-yl)acetic acid (_OX-COOH_), OX-COOH glucuronide, 3-(piperazine-1-yl)-1,2-benzisothiazole (_BITP_), BITP sulfoxide, BITP sulfone, BITP sulfone lactam, S-Methyl-dihydro-ziprasidone, S-Methyl-dihydro-ziprasidone-sulfoxide, 6-chloro-5-(2-piperazin-1-yl-ethyl)-1,3-dihydro-indol-2-one (_OX-P_), and dihydro-ziprasidone-sulfone. As suggested by the quantity of metabolites, ziprasidone is metabolized through several different pathways. Ziprasidone is sequentially oxidized to ziprasidone sulfoxide and ziprasidone sulfone, and oxidative N-dealkylation of ziprasidone produces OX-COOH and BITP. OX-COOH undergoes phase II metabolism to yield a glucuronidated metabolite while BITP is sequentially oxidized into BITP sulfoxide, BITP sulfone, then BITP sulfone lactam. Ziprasidone can also undergo reductive cleavage and methylation to produce S-Methyl-dihydro-ziprasidone and then further oxidation to produce S-Methyl-dihydro-ziprasidone-sulfoxide. Finally dearylation of ziprasidone produces OX-P, and the process of hydration and oxidation transforms the parent drug into dihydro-ziprasidone-sulfone. Although CYP3A4 and aldehyde oxidase are the primary enzymes involved in ziprasidone metabolism, the pathways associated with each enzyme have not been specified.
Ziprasidone is extensively metabolized in the liver principally via reduction by aldehyde oxidase with minimal excretion of unchanged drug in urine or feces. About one-third of ziprasidone's metabolic clearance is mediated by the cytochrome P-450 (CYP) 3A4 isoenzyme.
Ziprasidone is primarily cleared via three metabolic routes to yield four major circulating metabolites, benzisothiazole (BITP) sulphoxide, BITP-sulphone, ziprasidone sulphoxide, and S-methyl-dihydroziprasidone.
In vitro studies using human liver subcellular fractions indicate that S-methyl-dihydroziprasidone is generated in two steps. The data indicate that the reduction reaction is mediated by aldehyde oxidase and the subsequent methylation is mediated by thiol methyltransferase.
In vitro studies using human liver microsomes and recombinant enzymes indicate that CYP3A4 is the major CYP contributing to the oxidative metabolism of ziprasidone. CYP1A2 may contribute to a much lesser extent. Based on in vivo abundance of excretory metabolites, less than one-third of ziprasidone metabolic clearance is mediated by cytochrome P450 catalyzed oxidation and approximately two-thirds via reduction by aldehyde oxidase. There are no known clinically relevant inhibitors or inducers of aldehyde oxidase.
The metabolism and excretion of ziprasidone (5-[2-[4-(1,2-benzisothiazol-3-yl)piperazin-1-yl]ethyl]-6-+++chloroindolin-2-one hydrochloride hydrate) were studied in Long Evans rats after oral administration of a single dose of a mixture of 14C- and 3H-labeled ziprasidone. ... Ziprasidone was extensively metabolized in rats, and only a small amount of ziprasidone was excreted as unchanged drug. Twelve metabolites were identified ... The structures of eight metabolites were unambiguously confirmed by coelution on HPLC with synthetic standards, and four additional metabolites were partially identified. There was a gender-related difference in the excretion of urinary metabolites in Long Evans rats. The major route of metabolism in male rats involved N-dealkylation. In female rats the major metabolites were due to oxidation at the benzisothiazole ring. Based on the structures of these metabolites, four major and two minor routes of metabolism of ziprasidone were identified. The major routes included 1) N-dealkylation of the ethyl side chain attached to the piperazinyl nitrogen, 2) oxidation at the sulfur, resulting in the formation of sulfoxide and sulfone, 3) oxidation on the benzisothiazole moiety (other than sulfur), and 4) hydration of the C==N bond and subsequent oxidation at the sulfur of the benzisothiazole moiety. The minor routes involved N-oxidation on the piperazine ring and hydrolysis of the oxindole moiety.
Ziprasidone has known human metabolites that include 6-Chloro-5-ethyl-1,3-dihydroindol-2-one, 3-(1-Piperazinyl)-1,2-benzisothiazole, and Ziprasidone Sulfoxide.
Biological Half-Life
The half life of ziprasidone is 6-7 hours.
Elimination of ziprasidone is mainly via hepatic metabolism with a mean terminal half-life of about 7 hours within the proposed clinical dose range.
The mean t(1/2), z in the young men, young women, elderly men and elderly women were 3.1, 4.1, 5.7 and 5.3 hr, respectively.
Toxicity/Toxicokinetics
Toxicity Summary
IDENTIFICATION AND USE: Ziprasidone is indicated for the treatment of schizophrenia. Ziprasidone is indicated as monotherapy for the acute treatment of manic or mixed episodes associated with bipolar I disorder. Ziprasidone is indicated as an adjunct to lithium or valproate for the maintenance treatment of bipolar I disorder. HUMAN EXPOSURE AND TOXICITY: In the patient taking the largest confirmed amount, 3240 mg, the only symptoms reported were minimal sedation, slurring of speech, and transitory hypertension (200/95). In post-marketing use, adverse events reported in association with ziprasidone overdose generally included extrapyramidal symptoms, somnolence, tremor, and anxiety. Previously reported pediatric ziprasidone overdoses describe a syndrome of sedation, tachycardia, hypotonia, and coma. In pediatric ziprasidone overdose, QTc prolongation and hypotension have also been illustrated, but seizures have not been reported. An interesting case of ziprasidone intoxication involving the development of pinpoint pupils unresponsive to naloxone has been reported. This phenomenon has been reported before with overdose of olanzapine, a similar atypical antipsychotic. The mechanism of miosis associated with overdose of atypical antipsychotics is unclear but is likely related to interference with central innervation of the pupil. Geriatric patients with dementia-related psychosis treated with atypical antipsychotic drugs appear to be at an increased risk of death compared with that among patients receiving placebo. In one study, oral ziprasidone prolonged the QT interval on ECG by a mean of 9-14 msec more than that observed in patients receiving risperidone, olanzapine, quetiapine, or haloperidol, but approximately 14 msec less than that observed in patients receiving thioridazine. A ziprasidone overdose with quantitative serum levels of a pediatric patient in coma and with pinpoint pupils illustrating that ingestion of just 1 pill may result to profound mental status and respiratory depression in a child. Positive results were obtained in an in vitro chromosomal aberration assay in human lymphocytes. Psychiatric patients treated with atypical antipsychotic medications should be closely monitored for rhabdomyolysis during correction of hyponatremia, thus permitting prompt therapy to limit its complications. ANIMAL STUDIES: Lifetime carcinogenicity studies were conducted with ziprasidone in rats and mice. Ziprasidone was administered for 24 months in the diet at doses of 2, 6, or 12 mg/kg/day to rats, and 50, 100, or 200 mg/kg/day to mice (0.1 to 0.6 and 1 to 5 times the maximum recommended human dose [MRHD] of 200 mg/day on a sq m basis, respectively). In the rat study, there was no evidence of an increased incidence of tumors compared to controls. In male mice, there was no increase in incidence of tumors relative to controls. In female mice, there were dose-related increases in the incidences of pituitary gland adenoma and carcinoma, and mammary gland adenocarcinoma at all doses tested (50 to 200 mg/kg/day or 1 to 5 times the MRHD on an mg/sq m basis). Proliferative changes in the pituitary and mammary glands of rodents have been observed following chronic administration of other antipsychotic agents and are considered to be prolactin-mediated. Increases in serum prolactin were observed in a 1-month dietary study in female, but not male, mice at 100 and 200 mg/kg/day (or 2.5 and 5 times the MRHD on an mg/sq m basis). Ziprasidone had no effect on serum prolactin in rats in a 5-week dietary study at the doses that were used in the carcinogenicity study. Ziprasidone failed to induce significant weight gain during weeks 1-3, however, significant weight gain was observed on day 28 at 2.5 mg/kg (p < 0.05). Ziprasidone had no effect on food intake at any time point. A significant reduction in water intake (p < 0.05) was observed during the first week of treatment with 2.5 mg/kg ziprasidone. Ziprasidone had no effect on intra-abdominal fat weight, wet or dry uterine weight or plasma prolactin levels. All ziprasidone treated animals displayed a normal four-day estrous cycle. In rats, embryofetal toxicity (decreased fetal weights, delayed skeletal ossification) was observed following administration of 10 to 160 mg/kg/day during organogenesis or throughout gestation, but there was no evidence of teratogenicity. Doses of 40 and 160 mg/kg/day were associated with maternal toxicity. Ziprasidone was tested in the Ames bacterial mutation assay, the in vitro mammalian cell gene mutation mouse lymphoma assay, and the in vivo chromosomal aberration assay in mouse bone marrow. There was a reproducible mutagenic response in the Ames assay in one strain of S. typhimurium in the absence of metabolic activation. Positive results were obtained in the in vitro mammalian cell gene mutation assay.
Interactions
In vivo studies have revealed an approximately 35% decrease in ziprasidone AUC by concomitantly administered carbamazepine, an approximately 35-40% increase in ziprasidone AUC by concomitantly administered ketoconazole, but no effect on ziprasidone's pharmacokinetics by cimetidine or antacid.
Pharmacokinetic/pharmacodynamic studies between ziprasidone and other drugs that prolong the QT interval have not been performed. An additive effect of ziprasidone and other drugs that prolong the QT interval cannot be excluded. Therefore, ziprasidone should not be given with dofetilide, sotalol, quinidine, other Class Ia and III anti-arrhythmics, mesoridazine, thioridazine, chlorpromazine, droperidol, pimozide, sparfloxacin, gatifloxacin, moxifloxacin, halofantrine, mefloquine, pentamidine, arsenic trioxide, levomethadyl acetate, dolasetron mesylate, probucol or tacrolimus. Ziprasidone is also contraindicated with drugs that have demonstrated QT prolongation as one of their pharmacodynamic effects and have this effect described in the full prescribing information as a contraindication or a boxed or bolded warning.
Because of its potential for inducing hypotension, ziprasidone may enhance the effects of certain antihypertensive agents.
Ziprasidone may antagonize the effects of levodopa and dopamine agonists.
For more Interactions (Complete) data for Ziprasidone (8 total), please visit the HSDB record page.
References

[1]. 5-HT(1A) receptor activation contributes to ziprasidone-induced dopamine release in the rat prefrontal cortex. Biol Psychiatry. 2000;48(3):229-237.

[2]. Block of hERG channel by ziprasidone: biophysical properties and molecular determinants. Biochem Pharmacol. 2006 Jan 12;71(3):278-86.

[3]. The effect of ziprasidone on body weight and energy expenditure in female rats. Metabolism. 2012 Jun;61(6):787-93.

Additional Infomation
Therapeutic Uses
Antipsychotic Agents; Dopamine Antagonists; Serotonin Antagonists
Ziprasidone is indicated for the treatment of schizophrenia. The efficacy of oral ziprasidone was established in four short-term (4- and 6-week) controlled trials of adult schizophrenic inpatients and in one maintenance trial of stable adult schizophrenic inpatients. /Included in US product label/
Ziprasidone is indicated as monotherapy for the acute treatment of manic or mixed episodes associated with bipolar I disorder. Efficacy was established in two 3-week monotherapy studies in adult patients /Included in US product label/
Ziprasidone is indicated as an adjunct to lithium or valproate for the maintenance treatment of bipolar I disorder. Efficacy was established in a maintenance trial in adult patients. The efficacy of ziprasidone as monotherapy for the maintenance treatment of bipolar I disorder has not been systematically evaluated in controlled clinical trials /Included in US product label/
Drug Warnings
/BOXED WARNING/ WARNING: INCREASED MORTALITY IN ELDERLY PATIENTS WITH DEMENTIA-RELATED PSYCHOSIS. Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death. Analyses of seventeen placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1.6 to 1.7 times the risk of death in placebo-treated patients. Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group. Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature. Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality. The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic(s) of the patients is not clear. Ziprasidone is not approved for the treatment of patients with Dementia-Related Psychosis.
Contraindications /include/ known history of QT prolongation (including congenital long QT syndrome), recent acute myocardial infarction, or uncompensated heart failure. Concomitant therapy with other drugs that prolong the QT interval. Known hypersensitivity to ziprasidone.
Geriatric patients with dementia-related psychosis treated with atypical antipsychotic drugs appear to be at an increased risk of death compared with that among patients receiving placebo. Analyses of seventeen placebo-controlled trials (average duration of 10 weeks) revealed an approximate 1.6 - to 1.7-fold increase in mortality among geriatric patients receiving atypical antipsychotic drugs (ie, aripiprazole, olanzapine, quetiapine, risperidone) compared with that in patients receiving placebo. Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5% compared with a rate of about 2.6% in the placebo group. Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (eg, heart failure, sudden death) or infectious (eg, pneumonia) in nature. The manufacturer states that ziprasidone is not approved for the treatment of patients with dementia-related psychosis.
Prolongation of the QT interval can result in an occurrence of ventricular arrhythmias (eg, torsades de pointes) and/or sudden death. In one study, oral ziprasidone prolonged the QT interval on ECG by a mean of 9-14 msec more than that observed in patients receiving risperidone, olanzapine, quetiapine, or haloperidol, but approximately 14 msec less than that observed in patients receiving thioridazine. ... Patients at particular risk of torsades de pointes and/or sudden death include those with bradycardia, hypokalemia, or hypomagnesemia, those receiving concomitant therapy with other drugs that prolong the QTC interval, and those with congenital prolongation of QTC interval. The manufacturer states that ziprasidone should be avoided in patients with congenital prolongation of the QT interval or a history of cardiac arrhythmias and in those receiving concomitant therapy with other drugs that prolong the QTC interval.
For more Drug Warnings (Complete) data for Ziprasidone (28 total), please visit the HSDB record page.
Pharmacodynamics
Ziprasidone is classified as a "second generation" or "atypical" antipsychotic and is a dopamine and 5HT2A receptor antagonist with a unique receptor binding profile. As previously mentioned, ziprasidone has a very high 5-HT2A/D2 affinity ratio, binds to multiple serotonin receptors in addition to 5-HT2A, and blocks monoamine transporters which prevents 5HT and NE reuptake. On the other hand, ziprasidone has a low affinity for muscarinic cholinergic M1, histamine H1, and alpha1-adrenergic receptors.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C21H21CLN4OS
Molecular Weight
412.94
Exact Mass
412.11
Elemental Analysis
C, 61.08; H, 5.13; Cl, 8.58; N, 13.57; O, 3.87; S, 7.76
CAS #
146939-27-7
Related CAS #
Ziprasidone-d8; 1126745-58-1; Ziprasidone hydrochloride monohydrate; 138982-67-9; Ziprasidone hydrochloride; 122883-93-6; Ziprasidone mesylate trihydrate; 199191-69-0; Ziprasidone mesylate; 185021-64-1
PubChem CID
60854
Appearance
White to off-white solid powder
Density
1.4±0.1 g/cm3
Boiling Point
554.8±50.0 °C at 760 mmHg
Melting Point
213-215°C
Flash Point
289.3±30.1 °C
Vapour Pressure
0.0±1.5 mmHg at 25°C
Index of Refraction
1.681
LogP
4
Hydrogen Bond Donor Count
1
Hydrogen Bond Acceptor Count
5
Rotatable Bond Count
4
Heavy Atom Count
28
Complexity
573
Defined Atom Stereocenter Count
0
SMILES
ClC1C([H])=C2C(C([H])([H])C(N2[H])=O)=C([H])C=1C([H])([H])C([H])([H])N1C([H])([H])C([H])([H])N(C2C3=C([H])C([H])=C([H])C([H])=C3SN=2)C([H])([H])C1([H])[H]
InChi Key
MVWVFYHBGMAFLY-UHFFFAOYSA-N
InChi Code
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)
Chemical Name
5-[2-[4-(1,2-benzothiazol-3-yl)piperazin-1-yl]ethyl]-6-chloro-1,3-dihydroindol-2-one
Synonyms
CP 88059; CP88059; CP-88,059-01; CP88059 hydrochloride; CP-88059; CP-88,059; Ziprasidone HCl; Geodon; Zeldox; Zipwell
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: ~13.5 mg/mL (~32.7 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 1.35 mg/mL (3.27 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 13.5 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 1.35 mg/mL (3.27 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 13.5 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

View More

Solubility in Formulation 3: ≥ 1.35 mg/mL (3.27 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 13.5 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.4217 mL 12.1083 mL 24.2166 mL
5 mM 0.4843 mL 2.4217 mL 4.8433 mL
10 mM 0.2422 mL 1.2108 mL 2.4217 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

Calculator

Molarity Calculator allows you to calculate the mass, volume, and/or concentration required for a solution, as detailed below:

  • Calculate the Mass of a compound required to prepare a solution of known volume and concentration
  • Calculate the Volume of solution required to dissolve a compound of known mass to a desired concentration
  • Calculate the Concentration of a solution resulting from a known mass of compound in a specific volume
An example of molarity calculation using the molarity calculator is shown below:
What is the mass of compound required to make a 10 mM stock solution in 5 ml of DMSO given that the molecular weight of the compound is 350.26 g/mol?
  • Enter 350.26 in the Molecular Weight (MW) box
  • Enter 10 in the Concentration box and choose the correct unit (mM)
  • Enter 5 in the Volume box and choose the correct unit (mL)
  • Click the “Calculate” button
  • The answer of 17.513 mg appears in the Mass box. In a similar way, you may calculate the volume and concentration.

Dilution Calculator allows you to calculate how to dilute a stock solution of known concentrations. For example, you may Enter C1, C2 & V2 to calculate V1, as detailed below:

What volume of a given 10 mM stock solution is required to make 25 ml of a 25 μM solution?
Using the equation C1V1 = C2V2, where C1=10 mM, C2=25 μM, V2=25 ml and V1 is the unknown:
  • Enter 10 into the Concentration (Start) box and choose the correct unit (mM)
  • Enter 25 into the Concentration (End) box and select the correct unit (mM)
  • Enter 25 into the Volume (End) box and choose the correct unit (mL)
  • Click the “Calculate” button
  • The answer of 62.5 μL (0.1 ml) appears in the Volume (Start) box
g/mol

Molecular Weight Calculator allows you to calculate the molar mass and elemental composition of a compound, as detailed below:

Note: Chemical formula is case sensitive: C12H18N3O4  c12h18n3o4
Instructions to calculate molar mass (molecular weight) of a chemical compound:
  • To calculate molar mass of a chemical compound, please enter the chemical/molecular formula and click the “Calculate’ button.
Definitions of molecular mass, molecular weight, molar mass and molar weight:
  • Molecular mass (or molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
  • Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
/

Reconstitution Calculator allows you to calculate the volume of solvent required to reconstitute your vial.

  • Enter the mass of the reagent and the desired reconstitution concentration as well as the correct units
  • Click the “Calculate” button
  • The answer appears in the Volume (to add to vial) box
In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
Step 2: Enter in vivo formulation (This is only a calculator, not the exact formulation for a specific product. Please contact us first if there is no in vivo formulation in the solubility section.)
+
+
+

Calculation results

Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
             (2) Be sure to add the solvent(s) in order.

Clinical Trial Information
A Study to Assess the Safety and Efficacy of ASP4345 as Add-on Treatment for Cognitive Impairment in Subjects With Schizophrenia on Stable Doses of Antipsychotic Medication
CTID: NCT03557931
Phase: Phase 2    Status: Completed
Date: 2024-11-12
Ziprasidone in Early Onset Schizophrenia Spectrum Disorders
CTID: NCT01006551
Phase: Phase 2    Status: Completed
Date: 2024-08-15
Longitudinal Comparative Effectiveness of Bipolar Disorder Therapies
CTID: NCT02893371
Phase:    Status: Terminated
Date: 2024-03-12
Ziprasidone in the Psychosis Prodrome
CTID: NCT00635700
Phase: Phase 2    Status: Completed
Date: 2023-03-27
Proposal To Develop A Rapid And Cost-Effective Diagnostic Test For Schizophrenia
CTID: NCT03781115
Phase: Phase 1    Status: Unknown status
Date: 2022-02-24
View More

An Observational Drug Utilization Study of Asenapine in the United Kingdom (P08308)
CTID: NCT01498770
Phase:    Status: Completed
Date: 2022-02-04


Extension Study Evaluating The Safety And Tolerability Of Flexible Doses Of Oral Ziprasidone In Children And Adolescents With Bipolar I Disorder
CTID: NCT03768726
Phase: Phase 3    Status: Terminated
Date: 2021-06-16
Efficacy and Safety Trial of Flexible Doses of Oral Ziprasidone in Children and Adolescents With Bipolar I Disorder
CTID: NCT02075047
Phase: Phase 3    Status: Terminated
Date: 2021-06-16
A Six-week Flexible Dose Study Evaluating the Efficacy and Safety of Geodon in Patients With Bipolar I Depression.
CTID: NCT00282464
Phase: Phase 3    Status: Completed
Date: 2021-03-29
3-week Study to Evaluate Efficacy and Safety of Ziprasidone With Either Lithium or Divalproex in Acutely Manic Subjects
CTID: NCT00312494
Phase: Phase 3    Status: Completed
Date: 2021-03-29
Study Evaluating The Safety, Tolerability, And Efficacy Of Switching From Quetiapine To Ziprasidone
CTID: NCT00406315
Phase: Phase 4    Status: Completed
Date: 2021-03-29
Safety and Maintenance of Effect of Ziprasidone Plus a Mood Stabilizer in Bipolar I Disorder (Manic or Mixed)
CTID: NCT00280566
Phase: Phase 3    Status: Completed
Date: 2021-03-25
Safety and Tolerability of Ziprasidone in Children and Adolescents With Bipolar I Disorder (Manic or Mixed)
CTID: NCT00265330
Phase: Phase 3    Status: Completed
Date: 2021-03-25
A Six-Week Study Evaluating The Efficacy And Safety Of Geodon In Patients With A Diagnosis Of Bipolar I Depression
CTID: NCT00141271
Phase: Phase 3    Status: Completed
Date: 2021-03-25
Safety And Efficacy Of Ziprasidone In Adolescents With Schizophrenia
CTID: NCT00257192
Phase: Phase 3    Status: Terminated
Date: 2021-03-25
Extension Study of Patients Successfully Treated by Ziprasidone in Study A1281031
CTID: NCT00174447
Phase: Phase 3    Status: Completed
Date: 2021-03-24
Treatment of Schizophrenic Patients With Ziprasidone
CTID: NCT00579670
Phase:    Status: Completed
Date: 2021-03-10
Adjunctive Ziprasidone in the Treatment of Bipolar I Depression
CTID: NCT00483548
Phase: Phase 3    Status: Completed
Date: 2021-03-10
Safety and Efficacy of Ziprasidone in Children and Adolescents With Bipolar I Disorder (Manic or Mixed)
CTID: NCT00257166
Phase: Phase 3    Status: Completed
Date: 2021-03-03
Extension Study: Evaluating the Safety of Oral Ziprasidone in the Treatment of Subjects With Schizophrenia
CTID: NCT00139737
Phase: Phase 3    Status: Completed
Date: 2021-03-03
A Non-Interventional Post-Marketing Surveillance Study to Evalua
Randomized multicentric open-label phase III clinical trial to evaluate the efficacy of continual treatment versus discontinuation based in the presence of prodromes in a first episode of non-affective psychosis.
CTID: null
Phase: Phase 3    Status: Prematurely Ended
Date: 2012-06-08
Study to compare the efficacy of ziprasidone (Zeldox) and aripiprazole (Abilify) on cognitive functioning and quality of sleep in the treatment of schizophrenic patients
CTID: null
Phase: Phase 4    Status: Completed
Date: 2007-12-20
A SIXTEEN-WEEK, MULTI-CENTER, OPEN-LABEL STUDY EVALUATING THE SAFETY, TOLERABILITY, AND EFFICACY OF SWITCHING FROM QUETIAPINE TO ZIPRASIDONE IN SUBJECTS DIAGNOSED WITH SCHIZOPHRENIA OR SCHIZOAFFECTIVE DISORDER
CTID: null
Phase: Phase 4    Status: Completed
Date: 2006-12-08
Zur Frage des neuroleptikainduzierten metabolischen Syndroms.
CTID: null
Phase: Phase 4    Status: Completed
Date: 2006-09-21
Zur Frage des neuroleptikainduzierten metabolischen Syndroms.
CTID: null
Phase: Phase 4    Status: Completed
Date: 2006-09-20
Ziprasidone for severe conduct and other disruptive behavior disorders in children and adolescents – a placebo controlled, randomized, double blind clinical trial
CTID: null
Phase: Phase 2    Status: Completed
Date: 2006-06-29
A MULTICENTER, RANDOMIZED, DOUBLE-BLIND, PARALLEL GROUP STUDY, COMPARING THE EFFICACY AND TOLERABILITY OF ZIPRASIDONE (ZELDOX®, GEODON®) VS OLANZAPINE (ZYPREXA®) IN THE TREATMENT AND MAINTENANCE OF RESPONSE IN PATIENTS WITH ACUTE MANIA
CTID: null
Phase: Phase 3    Status: Prematurely Ended, Completed
Date: 2006-06-23
26-week open-label extension study evaluating the safety and tolerability of flexible doses of oral ziprasidone in adolescent subjects with schizophrenia.
CTID: null
Phase: Phase 3    Status: Prematurely Ended
Date: 2006-05-04
Six week, double-blind, placebo controlled Phase III trial evaluating the efficacy, safety and pharmacokinetics of flexible doses of oral ziprasidone in adolescent subjects with schizophrenia.
CTID: null
Phase: Phase 3    Status: Prematurely Ended
Date: 2006-05-04
A Phase 3, randomized, 6-month, double blind trial in subjects with Bipolar I Disorder to evaluate the continued safety and maintenance of effect of Ziprasidone plus a mood stabilizer (vs placebo plus a mood stabilizer) following a minimum of 4 months of response to open-label treatment with both agents.
CTID: null
Phase: Phase 3    Status: Completed
Date: 2006-01-25
Efficacy and tolerability of Ziprasidone vs. Clozapine in the treatment of dually diagnosed (DD-) patients with schizophrenia and cannabis use disorder: A randomised study
CTID: null
Phase: Phase 4    Status: Ongoing
Date: 2005-12-01
Effects of ziprasidone vs. placebo during the first four weeks of eight weeks sertraline treatment in patients with posttraumatic stress disorder (PTSD)
CTID: null
Phase: Phase 2    Status: Ongoing
Date: 2005-10-31
Influence of treatment of olanzapine and ziprasidone on transcapillary glucose transport in human skeletal muscle
CTID: null
Phase: Phase 4    Status: Completed
Date: 2005-05-26
Ensayo clínico con Ziprasidona para el tratamiento de la psicopatología no constituyente de un trastorno mental grave en la dependencia del alcohol
CTID: null
Phase: Phase 2    Status: Ongoing
Date: 2004-07-14
Hirnaktivierung während Gedächtnisaufgaben bei Patienten mit Schizophrenie unter Behandlung von Ziprasidon oder Risperidon. Eine FMRT-Untersuchung.
CTID: null
Phase: Phase 4    Status: Prematurely Ended
Date:

Contact Us