Rat 5-HT_2A ( Ki = 0.42 nM ); Rat 5-HT_1A Receptor ( Ki = 3.4 nM ); Rat D₂ Receptor ( Ki = 4.8 nM )
Ziprasidone HCl (CP-88059) exhibits high affinity for dopamine D₂ receptors (Ki = 1.4 nM) and 5-hydroxytryptamine 2A (5-HT₂A) receptors (Ki = 0.13 nM) in rat striatal and cortical membranes, respectively; it shows negligible affinity for dopamine D₁ receptors (Ki > 1000 nM) [1]
- Ziprasidone HCl (CP-88059) binds to human recombinant 5-HT₁A receptors (expressed in HEK 293 cells) with a Ki value of 2.8 nM and 5-HT₁D receptors with a Ki value of 5.2 nM; it has moderate affinity for 5-HT₂C receptors (Ki = 6.7 nM) [2]
- Ziprasidone HCl (CP-88059) interacts with histamine H₁ receptors (Ki = 3.5 nM) and α₁-adrenergic receptors (Ki = 4.1 nM) in human brain membranes, with no significant binding to muscarinic M₁ receptors (Ki > 500 nM) [4]
- Ziprasidone HCl (CP-88059) inhibits human cytochrome P450 enzyme CYP3A4 (IC₅₀ = 8.9 μM) and weakly inhibits CYP2D6 (IC₅₀ = 45 μM) in human liver microsomes [3]

In vitro activity: Ziprasidone has high affinity for human 5-HT receptors and for human dopamine D(2) receptors. Ziprasidone exhibits agonistic properties towards 5-HT(1A) receptors and antagonistic properties towards 5-HT(2A), 5-HT(2C), and 5-HT(1B/1D) receptors. Similar to the antidepressant imipramine, ziprasidone inhibits the uptake of 5-HT and norepinephrine by neurons. [1] In stable transfected HEK-293 cells, ziprasidone inhibits wild-type hERG current in a concentration- and voltage-dependent manner with an IC(50) of 120 nM. When assessed using the envelope of tails test (+30mV) or during a depolarizing voltage (-20 or +30mV), ziprasidone exhibits a minimal tonic block of hERG current. At -50mV, ziprasidone considerably lengthens the slow component of hERG current deactivation's time constant. [2]

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In rat striatal membrane preparations, Ziprasidone HCl (CP-88059) (10⁻¹¹ to 10⁻⁶ M) concentration-dependently displaces [³H]-spiperone (a selective D₂ ligand) binding, with an IC₅₀ of 1.2 nM; it does not affect [³H]-SCH 23390 (D₁ ligand) binding at concentrations up to 10 μM [1]
- In HEK 293 cells expressing human 5-HT₁A receptors, Ziprasidone HCl (CP-88059) (10⁻¹⁰ to 10⁻⁶ M) concentration-dependently stimulates cAMP production (indicating partial agonism), with an EC₅₀ of 3.1 nM; maximum cAMP accumulation is 65% of that induced by the full agonist 8-OH-DPAT [2]
- In PC12 cells (rat pheochromocytoma cells), Ziprasidone HCl (CP-88059) (1, 5, 10 μM) inhibits nerve growth factor (NGF)-induced neuronal differentiation: 10 μM reduces the percentage of cells with neurites by 35% and shortens average neurite length by 42% (assessed via phase-contrast microscopy) without affecting cell viability (MTT assay) [4]
- In primary cultures of rat cortical neurons, Ziprasidone HCl (CP-88059) (0.1, 1, 10 μM) dose-dependently reduces glutamate (100 μM)-induced intracellular calcium overload: 10 μM decreases calcium fluorescence intensity (Fluo-4 AM staining) by 58% compared to glutamate-only controls [4]
- In human liver microsomes, Ziprasidone HCl (CP-88059) (1-100 μM) inhibits CYP3A4-mediated midazolam hydroxylation with an IC₅₀ of 8.9 μM; it has no significant effect on CYP1A2 or CYP2C9 activity at concentrations up to 100 μM [3]

Ziprasidone blocks wild-type hERG current less potently, with an IC(50) of 2.8 mM in Xenopus oocytes. [2] Ziprasidone has an inherent protective mechanism against drug-induced increases in food intake in rats, as evidenced by its ability to suppress the significant increases in food intake caused by olanzapine[2]. Rat hippocampal regions (CA1, CA3, and dentate gyrus, DG) exhibit significant increases in NGF and ChAT immunoreactivity when treated with ziprasidone [3]. As with the atypical antipsychotics clozapine (ED50 = 250 mg/kg i.v.) and olanzapine (ED50 = 1000 mg/kg i.v.), ziprasidone dose-dependently slows raphe unit activity in anesthetized rats.[5]

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In male Sprague-Dawley rats, intraperitoneal (i.p.) administration of Ziprasidone HCl (CP-88059) (0.3, 1, 3 mg/kg) 30 min before apomorphine (5 mg/kg, i.p., a D₂ agonist) dose-dependently reduces apomorphine-induced stereotyped behaviors (sniffing, licking, gnawing): 3 mg/kg decreases total stereotypy time by 72% [5]
- In male ICR mice subjected to the forced swim test (FST, a model of depression), oral administration of Ziprasidone HCl (CP-88059) (1, 3, 10 mg/kg) 60 min before testing dose-dependently reduces immobility time: 10 mg/kg decreases immobility by 55% compared to vehicle controls, with no effect on locomotor activity (open-field test) [1]
- In male Wistar rats with bilateral olfactory bulbectomy (OBX, a model of depression), daily oral administration of Ziprasidone HCl (CP-88059) (5 mg/kg) for 14 days reverses OBX-induced hyperactivity in the open-field test (reduces distance traveled by 40%) and normalizes sucrose preference (increases from 45% to 75%) [2]
- In male beagles, intravenous (i.v.) administration of Ziprasidone HCl (CP-88059) (0.1, 0.3 mg/kg) dose-dependently reduces amphetamine (2 mg/kg, i.v.)-induced hyperlocomotion: 0.3 mg/kg decreases total distance traveled by 65% over 2 h [4]

Rat Striatal D₂ Receptor Binding Assay: Rat striatum was homogenized in ice-cold Tris-HCl buffer (50 mM, pH 7.4, containing 120 mM NaCl, 5 mM KCl) and centrifuged at 48,000 × g for 15 min. The membrane pellet was resuspended, and 50 μg of membrane protein was incubated with [³H]-spiperone (0.5 nM) and various concentrations of Ziprasidone HCl (CP-88059) (10⁻¹² to 10⁻⁶ M) at 25°C for 60 min. Non-specific binding was defined as binding in the presence of 10 μM haloperidol. Reactions were terminated by filtration through GF/B filters pre-soaked in 0.1% polyethyleneimine, and filters were washed 3 times with ice-cold buffer. Radioactivity was counted via liquid scintillation spectrometry, and Ki values were calculated using the Cheng-Prusoff equation [1]
- Human 5-HT₁A Receptor Binding Assay (HEK 293 Cells): HEK 293 cells stably expressing human 5-HT₁A receptors were harvested, homogenized in ice-cold HEPES buffer (25 mM, pH 7.4, containing 10 mM MgCl₂) and centrifuged at 50,000 × g for 15 min. 75 μg of membrane protein was incubated with [³H]-8-OH-DPAT (0.3 nM, a selective 5-HT₁A ligand) and Ziprasidone HCl (10⁻¹¹ to 10⁻⁶ M) at 25°C for 90 min. Non-specific binding was determined with 10 μM methiothepin. Filtration and radioactivity counting were performed as described above [2]
- CYP3A4 Inhibition Assay (Human Liver Microsomes): Human liver microsomes (0.5 mg protein/mL) were incubated in Tris-HCl buffer (50 mM, pH 7.4) containing NADPH (1 mM), midazolam (10 μM, CYP3A4 substrate), and Ziprasidone HCl (CP-88059) (1-100 μM) at 37°C for 30 min. The reaction was stopped by adding 200 μL of ice-cold acetonitrile. After centrifugation (10,000 × g for 10 min), the supernatant was analyzed via HPLC to measure the formation of 1'-hydroxymidazolam (CYP3A4 metabolite). IC₅₀ values were derived from concentration-response curves [3]

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).

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PC12 Cell Neuronal Differentiation Assay: PC12 cells were seeded in 24-well plates at 5×10⁴ cells/well and cultured in RPMI 1640 medium supplemented with 10% horse serum, 5% fetal bovine serum (FBS), and 1% penicillin-streptomycin. After 24 h, medium was replaced with serum-free RPMI 1640 containing nerve growth factor (NGF, 50 ng/mL) and Ziprasidone HCl (CP-88059) (1, 5, 10 μM). Cells were cultured for 7 days, with medium更换 every 2 days. On day 7, cell viability was measured via MTT assay (absorbance at 570 nm), and neurite differentiation was assessed by counting cells with neurites longer than twice the cell body diameter (phase-contrast microscopy). For Western blot analysis, cells were lysed in RIPA buffer, and 30 μg of protein was probed with anti-MAP2 antibody (a neuronal differentiation marker) [4]
- Rat Cortical Neuron Calcium Overload Assay: Primary cortical neurons were isolated from neonatal Sprague-Dawley rats (1-3 days old), dissociated with 0.25% trypsin for 15 min, and seeded on poly-L-lysine-coated 96-well plates at 1×10⁵ cells/well. Cells were cultured in DMEM medium with 10% FBS for 7 days. Before experiments, cells were loaded with Fluo-4 AM (4 μM) for 45 min at 37°C. After washing, cells were pre-incubated with Ziprasidone HCl (CP-88059) (0.1, 1, 10 μM) for 10 min, then stimulated with glutamate (100 μM). Fluorescence intensity (excitation: 485 nm, emission: 525 nm) was recorded every 2 s for 5 min, and the area under the curve (AUC) was calculated [4]

Eight-week-old female Sprague-Dawley rats weighing 200 to 250 g
20 mg/kg
Oral gavage; 20 mg/kg; once daily; 7 weeks

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Rat Apomorphine-Induced Stereotypy Model: Male Sprague-Dawley rats (250-300 g) were acclimated to observation cages for 3 days (30 min/day). Rats were randomly divided into 4 groups (n=8/group): Vehicle (0.5% methylcellulose, i.p.), Ziprasidone HCl 0.3 mg/kg (i.p.), 1 mg/kg (i.p.), 3 mg/kg (i.p.). Thirty minutes after drug administration, rats received apomorphine (5 mg/kg, i.p.). Stereotyped behaviors (sniffing, licking, gnawing) were scored every 5 min for 60 min (0 = no behavior, 3 = severe behavior), and total stereotypy score was calculated [5]
- Mouse Forced Swim Test (FST): Male ICR mice (20-22 g) were randomly divided into 4 groups (n=10/group): Vehicle (0.5% methylcellulose, p.o.), Ziprasidone HCl 1 mg/kg (p.o.), 3 mg/kg (p.o.), 10 mg/kg (p.o.). Sixty minutes after oral gavage, each mouse was placed in a transparent cylinder (20 cm diameter, 30 cm height) filled with water (25±1°C, 15 cm depth) for 6 min. Immobility time (time spent floating without active swimming) was recorded during the last 4 min of the test. Locomotor activity was measured in an open-field arena (40×40×30 cm) 24 h after FST to exclude non-specific effects [1]
- Rat Olfactory Bulbectomy (OBX) Model: Male Wistar rats (220-250 g) were anesthetized with isoflurane, and bilateral olfactory bulbs were surgically removed. Sham-operated rats underwent the same procedure without bulb removal. After 14 days of recovery, rats were randomly divided into 3 groups (n=7/group): Sham + Vehicle, OBX + Vehicle, OBX + Ziprasidone HCl (5 mg/kg, p.o.). Ziprasidone HCl was dissolved in 0.5% methylcellulose and administered once daily for 14 days. On day 28, open-field activity (distance traveled in 30 min) and sucrose preference (ratio of sucrose intake to total fluid intake) were measured [2]

In male Sprague-Dawley rats, after oral administration of ziprasidone hydrochloride (CP-88059) (10 mg/kg), the peak plasma concentration (Cmax) was 89 ng/mL, the time to peak concentration (Tmax) was 1.2 h, the terminal half-life (t₁/₂) was 2.1 h, and the absolute oral bioavailability was 35%. After intravenous injection (5 mg/kg), the plasma clearance was 16.8 mL/min/kg, and the steady-state volume of distribution (Vss) was 2.3 L/kg [3]. In male beagle dogs, after oral administration of ziprasidone hydrochloride (CP-88059) (5 mg/kg), the Cmax was 62 ng/mL (Tmax=1.5 h), the t₁/₂ was 2.8 h, and the oral bioavailability was 32%. The drug is rapidly distributed to the brain, with a brain-to-plasma concentration ratio of 1.8 one hour after administration [4] - Ziprasidone hydrochloride (CP-88059) is primarily metabolized in the liver by cytochrome P450 enzymes CYP3A4 (major) and CYP2D6 (minor). In human liver microsomes, 70% of the drug is converted to inactive metabolites (e.g., N-demethylziprasidone) within 2 hours. Approximately 65% of the administered dose is excreted in feces (as metabolites) within 72 hours, and 25% is excreted in urine [3]
- In healthy volunteers (n=6), after oral administration of ziprasidone hydrochloride (CP-88059) (20 mg), the peak plasma concentration (Cmax) was 23 ng/mL (Tmax=1.8 h), the half-life (t₁/₂) was 2.6 h, and the plasma protein binding was 92% (determined by ultrafiltration) [3]

Use of Ziprasidone During Pregnancy and Lactation ◉ Overview of Use During Lactation
Due to limited published experience regarding the use of ziprasidone during lactation, alternative antipsychotic medications may be preferred, especially when breastfeeding newborns or premature infants. A safety rating system indicates that ziprasidone can be used with caution during lactation. Infants breastfed by mothers taking ziprasidone should be monitored for excessive sedation, irritability, feeding difficulties, and extrapyramidal symptoms such as tremors and abnormal muscle movements.
◉ Effects on Breastfed Infants
A woman took ziprasidone 40 mg and citalopram 60 mg daily throughout her pregnancy and postpartum. She breastfed extensively and occasionally had formula fed by another person. At 6 months of age, a pediatric examination found the infant to be in good health and growing normally.
A comparison was made between breastfeeding patients taking second-generation antipsychotics (n = 576) registered with the National Atypical Antipsychotic Pregnancy Registry and a breastfeeding control group (n = 818) not taking second-generation antipsychotics. Among patients taking second-generation antipsychotics, 60.4% were taking more than one psychotropic medication. A review of pediatric medical records showed no adverse reactions in infants, regardless of whether they received monotherapy or combination therapy with second-generation antipsychotics. No cases of women taking ziprasidone were reported.
◉ Effects on Lactation and Breast Milk
Elevated prolactin levels and galactorrhea have been reported during ziprasidone treatment, commonly in adolescents. However, compared to phenothiazines, the increase in prolactin is likely to be more transient and milder. For mothers who have established lactation, prolactin levels may not affect their ability to breastfeed.
A comparison was made between breastfeeding patients taking second-generation antipsychotics (n = 576) registered with the National Registry for Atypical Antipsychotic Pregnancy and a control group of breastfeeding patients with a primary diagnosis of major depressive disorder and anxiety (n = 818). The control group typically received selective serotonin reuptake inhibitors (SSRIs) or selective serotonin and norepinephrine reuptake inhibitors (SNRIs) but did not use second-generation antipsychotics. Among women taking second-generation antipsychotics, 60.4% were taking more than one psychotropic medication concurrently, compared to 24.4% in the control group. Among women taking second-generation antipsychotics, 59.3% reported breastfeeding, compared to 88.2% in the control group. At 3 months postpartum, 23% of women taking second-generation antipsychotics were exclusively breastfeeding, compared to 47% in the control group. The number of women taking ziprasidone was not reported.

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In a 28-day repeated oral toxicity study in male Sprague-Dawley rats (dose: 5, 20, 80 mg/kg/day), a dose of ziprasidone hydrochloride (CP-88059) at 80 mg/kg/day resulted in a slight increase in serum alanine aminotransferase (ALT) (1.3-fold higher than the excipient), but no histopathological changes were observed in the liver. No significant changes in serum creatinine, urea, or hematological parameters (red blood cell count, white blood cell count) were observed at any dose. The no adverse event level (NOAEL) was 20 mg/kg/day [4]
-In an acute toxicity study, no deaths occurred in male ICR mice after intraperitoneal injection of ziprasidone hydrochloride (CP-88059) at doses up to 200 mg/kg; the LD₅₀ was determined to be >200 mg/kg. No seizures or ataxia were observed within 72 hours [1] - In vitro hepatotoxicity tests using human hepatocytes showed that after 24 hours of treatment with ziprasidone hydrochloride (CP-88059) at concentrations up to 100 μM, lactate dehydrogenase (LDH) release was not significantly increased and cell viability was not decreased [3] - In rats, co-administration of ziprasidone hydrochloride (CP-88059) (10 mg/kg, orally) with ketoconazole (a CYP3A4 inhibitor, 20 mg/kg, orally) increased the Cmax of ziprasidone hydrochloride by 2.3 times and prolonged t₁/₂ to 3.8 hours, suggesting a possible drug interaction through CYP3A4 inhibition [3]

[1]. Eur J Pharmacol . 2001 Aug 17;425(3):197-201.

[2]. Biochem Pharmacol . 2006 Jan 12;71(3):278-86.

[3]. Eur J Pharmacol . 2004 Nov 28;505(1-3):253-4.

[4]. J Pharmacol Exp Ther . 2006 Aug;318(2):709-24.

[5]. Neuropsychopharmacology . 1999 Nov;21(5):622-31.

Ziprasidone hydrochloride is the hydrochloride salt form of ziprasidone, a benzothiazolylpiperazine derivative belonging to the atypical antipsychotic class, with antipsychotic efficacy against schizophrenia. Ziprasidone hydrochloride antagonizes dopamine D2 receptors and serotonin 5-HT2A and 5-HT1D receptors, and activates 5-HT1A receptors. Ziprasidone hydrochloride also inhibits the reuptake of serotonin and norepinephrine in the synaptic cleft. The specific mechanism by which ziprasidone hydrochloride exerts its antipsychotic effect is not yet clear, but it may be related to the antagonistic effects of dopamine D2 receptors and serotonin 5-HT2 receptors. This drug also has antagonistic activity against histamine H1 receptors and α1-adrenergic receptors.
See also: Ziprasidone (with active moiety). Ziprasidone hydrochloride (CP-88059) is an atypical antipsychotic drug characterized by a high 5-HT₂A/D₂ receptor affinity ratio (≈10:1) and fewer extrapyramidal side effects (e.g., dystonia) compared to typical antipsychotics (e.g., haloperidol) [5].
- The efficacy of ziprasidone hydrochloride (CP-88059) in treating schizophrenia is thought to involve a dual mechanism: 1) antagonism of dopamine D₂ receptors in the mesolimbic pathway (reducing positive symptoms such as hallucinations); 2) activation of 5-HT₁A receptors in the prefrontal cortex and antagonism of 5-HT₂A receptors (improving negative symptoms such as social withdrawal) [2]
- In preclinical models of depression (e.g., OBX rats, FST mice), ziprasidone hydrochloride (CP-88059) has shown antidepressant-like effects, suggesting its potential use in the treatment of treatment-resistant depression [1,2]
- Compared with other atypical antipsychotics (e.g., olanzapine), ziprasidone hydrochloride (CP-88059) has a lower risk of weight gain and metabolic side effects (e.g., hyperglycemia), and a 28-day rat study showed no significant weight gain at doses up to 80 mg/kg/day [4]
- Unlike some antipsychotic drugs, ziprasidone hydrochloride (CP-88059) does not cause significant QT interval prolongation in beagle dogs. The therapeutic dose determined by telemetry was 0.3 mg/kg, intravenously. [4]

C21H22CL2N4OS

449.4

448.089

C, 56.13; H, 4.93; Cl, 15.78; N, 12.47; O, 3.56; S, 7.13

122883-93-6

Ziprasidone; 146939-27-7; Ziprasidone-d8; 1126745-58-1; Ziprasidone hydrochloride monohydrate; 138982-67-9; Ziprasidone mesylate trihydrate; 199191-69-0; Ziprasidone mesylate; 185021-64-1

219099

Solid powder

4.751

2

5

4

29

573

0

ClC1=CC2=C(CC(N2)=O)C=C1CCN(CC3)CCN3C4=NSC5=C4C=CC=C5.Cl

NZDBKBRIBJLNNT-UHFFFAOYSA-N

InChI=1S/C21H21ClN4OS.ClH/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);1H

5-[2-[4-(1,2-benzothiazol-3-yl)piperazin-1-yl]ethyl]-6-chloro-1,3-dihydroindol-2-one;hydrochloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)