Mice exposed to respiratory toxicity caused by paraoxon can recover with a single intramuscular injection of pralidoxime iodide (10–150 mg/kg) [3].

Animal/Disease Models: Male F1B6D2 mice (diethyl paraoxon is toxic but not lethal in conscious, unrestrained mice) [3]
Doses: 10, 50, 100 and 150 mg/kg
Route of Administration: Results of a single intramuscularinjection: induced partial (albeit complete) reversal of respiratory toxicity at a dose of 50 mg/kg, and complete reversal of diethyl paraoxon-induced respiratory toxicity in mice at a dose of 150 mg/kg.

Absorption, Distribution and Excretion
This drug is rapidly excreted in the urine, partially unchanged and partially as hepatic metabolites. It is currently unclear whether pralidoxime can cross the human placenta into the embryo or fetus. Pralidoxime chloride is a quaternary ammonium compound, but the molecular weight of its free base (approximately 137) is low enough to cross the placenta. Rapid drug clearance should reduce this transport. A study involving 22 participants aimed to investigate the specific mechanisms by which renal tubules process pralidoxime (a quaternary ammonium compound used to reactivate cholinesterase, an inhibitor of organophosphates). During the study, each participant was under specific conditions. All 22 participants received pralidoxime (5 mg/kg, intravenously, over 2 minutes) under conditions of forced hydration and bed rest, serving as a control group. Eight participants received pralidoxime under conditions of forced hydration and bed rest, once after 36 hours of ammonium chloride acidification and another after sodium bicarbonate alkalization. Nine subjects received pralidoxime under forced dehydration and bed rest, followed by an intramuscular injection of thiamine (total dose 200 mg) 20–30 minutes later. Eight subjects received pralidoxime under forced hydration and bed rest, simultaneously receiving an intravenous injection of para-aminohippuric acid (total dose 900 mg). Four subjects received pralidoxime after 8–12 hours of bed rest and fasting. The drug is rapidly cleared from plasma via renal tubular secretion. Compared to para-aminohippuric acid administration, thiamine administration resulted in decreased clearance and a prolonged biological half-life of pralidoxime, indicating that it is secreted as an organic base. The reduced excretion of pralidoxime under urinary alkalinization and acidification conditions suggests previously undescribed active reabsorption. This study investigated the pharmacokinetics of pralidoxime chloride (2-PAM) in rats. Rats in different groups were intramuscularly injected with three doses (20, 40, or 80 mg/kg) of 2-PAM. This dosage range is commonly used to study the efficacy of 2-PAM in treating poisoning by potent organophosphorus cholinesterase inhibitors. During the experiment, continuous blood samples were collected from each rat. The plasma concentration of 2-PAM in each animal was measured over time. Then, a standard pharmacokinetic model was used to describe the relationship between plasma concentration and time. Estimates of various pharmacokinetic parameters were calculated using an open-cell, one-compartment model, including volume of distribution (Vd), maximum plasma concentration (Cmax), elimination rate constant (k10), absorption rate constant (k01), area under the curve (AUC), and clearance (CL). Only Cmax and AUC were statistically significant (p < 0.0001) when comparing all dosage groups; these pharmacokinetic parameters were highly correlated with dose, with correlation coefficients of r = 0.998 and r = 0.997, respectively. However, no significant differences were found in the transformed data after standardizing AUC and Cmax by the dose. The results from this study in rats indicate that the pharmacokinetics of 2-PAM are linearly related to the dose within the dose range used in the 2-PAM treatment studies. Background: Current treatments for organophosphate poisoning include the use of oximes, such as pralidoxime iodide (2-PAM), to reactivate acetylcholinesterase. Animal model studies have shown that 2-PAM concentrations in the brain are low after systemic injection. Methods: To assess 2-PAM transport, we investigated the transwell permeability of three Madin-Darby canine kidney (MDCKII) cell lines and stem cell-derived human brain microvascular endothelial cells (BC1-hBMECs). To determine whether 2-PAM is a substrate of common brain efflux pumps, we conducted experiments in the MDCKII-MDR1 cell line overexpressing the P-gp efflux pump and the MDCKII-FLuc-ABCG2 cell line overexpressing the BCRP efflux pump, respectively. To determine how transcellular transport affects enzyme reactivation, we developed a modified Transwell chamber assay in which an inhibited acetylcholinesterase, substrate, and reporter gene were introduced into the basolateral chamber. Paraoxon and parathion were used to inhibit enzyme activity. Results: 2-PAM permeability was approximately 2 × 10⁻⁶ cm/s in MDCK cells and approximately 1 × 10⁻⁶ cm/s in BC1-hBMEC cells. Atropine pretreatment did not affect its permeability. Furthermore, 2-PAM was not a substrate of the P-gp or BCRP efflux pump. Conclusion: Low permeability explains the poor brain permeability of 2-PAM, thus leading to slow enzyme reactivation. This elucidates one reason why continuous intravenous infusion is required in organophosphate poisoning.
For more complete data on the absorption, distribution, and excretion of 2-PAM (of 10), please visit the HSDB records page.

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Metabolism/Metabolites
Hepatic
While the exact metabolic pathway of pralidoxime is not fully elucidated, the drug is believed to be metabolized in the liver. …A recent study suggests that active tubular secretion may be involved, but the specific mechanism remains unclear.
Currently, the dosage of pralidoxime for treating organophosphate poisoning in humans is trending upwards, which may be related to certain specific populations. In fact, pralidoxime is primarily excreted unchanged via the kidneys. This study aimed to evaluate the effects of renal failure on the pharmacokinetics of pralidoxime in a rat model of potassium dichromate-induced acute renal failure. On day 1, Sprague-Dawley rats were subcutaneously injected with potassium dichromate (experimental group) or saline (control group). Forty-eight hours after injection, pralidoxime methyl sulfate (50 mg/kg pralidoxime base) was intramuscularly injected. Blood samples were collected within 180 minutes of injection. Urine was collected daily during the 3-day experiment. Plasma pralidoxime concentrations were determined using liquid chromatography-electrochemical detection. Compared to the control group, the mean elimination half-life in the study group increased by 2-fold, and the mean area under the curve increased by 2.5-fold. The mean systemic clearance in the study group was halved compared to the control group. Our study indicates that acute renal failure does not alter the distribution of pralidoxime, but it significantly alters its elimination from plasma. These results suggest that the pralidoxime dose should be adjusted when using high-dose pralidoxime treatment regimens in patients with organophosphate poisoning and renal failure.

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Biological Half-Life
74-77 minutes
The half-life of pralidoxime in patients with normal renal function varies among individuals, reportedly ranging from 0.8 to 2.7 hours.

Toxicity Summary
Identification and Uses: Pralidoxime is an antidote and cholinesterase reactivator used to treat poisoning caused by pesticides and chemicals with anticholinesterase activity. It is also used to treat overdose of anticholinesterase drugs used in the treatment of myasthenia gravis. In the context of chemical warfare or terrorism, pralidoxime chloride is used in combination with atropine to treat nerve agent poisoning. Pralidoxime chloride must be administered within minutes to hours after exposure to the nerve agent to be effective. Human Studies: Overdose in normal subjects manifests as dizziness, blurred vision, diplopia, headache, accommodation disorder, nausea, and mild tachycardia. It is difficult to distinguish between drug-induced and poison-induced side effects during treatment. When atropine is used in combination with pralidoxime chloride, atropinization symptoms (flushing, dilated pupils, tachycardia, dry mouth and nose) may appear earlier than expected when atropine is used alone. Animal Studies: Pralidoxime chloride is used to treat organophosphate poisoning; in dogs anesthetized with open-chest anesthesia, all doses significantly increased cardiac output. Similar responses were observed in alpha-adrenergic blockade animals, but not in β-adrenergic blockade or reserpine-treated animals. All doses of pralidoxime chloride significantly increased mean arterial pressure in the control, β-adrenergic blockade, and alpha-adrenergic blockade groups. Pralidoxime chloride at 20 mg/kg and 40 mg/kg also increased arterial pressure in reserpine-treated animals. Heart rate decreased in all animals treated with pralidoxime chloride except in the alpha-adrenergic blockade group. Total peripheral resistance increased with each administration of pralidoxime chloride in β-adrenergic blockade animals, while no significant increase was observed in the control group. The increase in total peripheral resistance was smaller in the reserpine-treated and alpha-adrenergic blockade groups. Stroke volume and stroke work increased significantly in all animals, and the atrial pressure at which these changes occurred varied among the different treatment groups. These results indicate that pralidoxime chloride directly stimulates cardiac and vascular smooth muscle. High doses of pralidoxime iodide in dogs can cause symptoms related to its own anticholinesterase activity. Clinical signs of toxicity in dogs may include muscle weakness, ataxia, vomiting, hyperventilation, seizures, respiratory arrest, and death. [hr] [protein binding] [not bound to plasma proteins] [hr] [interactions] This article describes the pharmacokinetics of 5 mg/kg pralidoxime iodide (Protopam I) administered intravenously one hour after continuous infusion of thiamine hydrochloride (II). Subjects received I alone or concurrently with II infusion. With the addition of II, urinary excretion of the oxime remained unchanged, but excretion decreased in the first 3 hours; the plasma half-life of the oxime was prolonged; plasma concentrations of the oxime increased; and intercompartmental clearance and elimination rate constants of the oxime decreased. The study concludes that compound II and the oxime compete for a common renal secretion mechanism, or compound II alters the membrane transport of the oxime. Background and Objectives: Treatment of organophosphate poisoning with pralidoxime requires improvement. This study investigated the pharmacokinetics of pralidoxime alone or in combination with avizafen and atropine using an autoinjector. Methods: This study employed an open-label, randomized, single-dose, two-way crossover design. At each cycle, each subject received an intramuscular injection of pralidoxime (700 mg) or two injections of the following combination: pralidoxime (350 mg), atropine (2 mg), and avizafen (20 mg). The concentration of pralidoxime was quantified using a validated liquid chromatography-tandem mass spectrometry (LC/MS-MS). Two methods were used to analyze these data: (i) a non-compartmental model; and (ii) a compartmental model method. Main Results: Compared with pralidoxime alone (beyond bioequivalence), pralidoxime in combination with atropine and avizafen resulted in a higher maximum concentration of pralidoxime, while the AUC values of pralidoxime were comparable. The maximum concentration of pralidoxime was reached more quickly after the combination injection. Based on the Akaike information criterion and goodness-of-fit criterion, the optimal model describing the pharmacokinetics of pralidoxime is a two-compartment model with zero-order absorption. When pralidoxime is co-administered with avizafone and atropine, the optimal model describing the pharmacokinetics becomes a two-compartment model with first-order absorption. Conclusions and Implications: Both non-compartmental and compartmental models demonstrate that, compared to pralidoxime alone, co-administration of avizafone and atropine with pralidoxime results in faster absorption into systemic circulation and a higher maximum plasma concentration. Our recent research has shown that pyridoxime compounds (the most well-known antidotes to chemical warfare nerve agents) can significantly detoxify the carcinogen tetrachloro-1,4-benzoquinone (TCBQ) through an unusual double Beckmann cleavage mechanism. However, it remains unclear why 2-PAM overdose does not completely protect the body from TCBQ-induced biological damage. This study unexpectedly discovered that TCBQ can also activate pralidoxime iodide, generating a reactive imine radical intermediate through a two-step sequential reaction. This intermediate was detected and clearly characterized using complementary techniques including electron spin resonance (ESR) spin trapping, high-performance liquid chromatography/mass spectrometry (HPLC/MS), and nitrogen-15 isotope labeling. The same imine radical was also observed when TCBQ was substituted with other haloquinones. The final product of the imine radical was isolated and identified as the corresponding reactive and toxic aldehyde. Based on these data, we propose that the reaction of 2-PAM with TCBQ may proceed through two competing pathways: nucleophilic attack of TCBQ by 2-PAM to form an unstable transient intermediate, which can undergo heterolytic cleavage via double Beckmann fracture to generate 2-CMP, or homolytic cleavage via two steps to generate a reactive imine radical, which subsequently undergoes hydrogen abstraction and further hydrolysis to generate the corresponding more toxic aldehyde. Similar homolytic cleavage mechanisms have also been observed in other haloquinones and pyridine aldehyde oximes. This study is the first to detect and identify reactive imine radical intermediates produced under normal physiological conditions, providing direct experimental evidence to explain the partial protective effect of 2-PAM against TCBQ-induced biological damage and the potential side effects of antidotes to 2-PAM and other pyridine oximes. When atropine and pralidoxime chloride are used in combination, the onset of atropinization symptoms (flushing, mydriasis, tachycardia, dry mouth, and dry nose) may be earlier than when atropine is used alone. This is especially true if the total dose of atropine is high and the administration of pralidoxime chloride is delayed. The following precautions should be taken when treating anticholinesterase poisoning, although these are not directly related to the use of pralidoxime chloride: barbiturates should be used with caution when treating seizures because their effects are enhanced by anticholinesterase; morphine, theophylline, aminophylline, reserpine, and phenothiazine sedatives should be avoided in patients with organophosphate poisoning. Reports indicate that succinylcholine, when used in combination with drugs possessing anticholinesterase activity, can cause persistent paralysis in patients; therefore, caution should be exercised when using it.

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Non-human toxicity values
Dog oral LD50: 190 mg/kg

[1]. Probing the activity of a non-oxime reactivator for acetylcholinesterase inhibited by organophosphorus nerve agents. Chem Biol Interact. 2016;259(Pt B):133‐141.

[2]. Eyer P, Buckley N. Pralidoxime for organophosphate poisoning. Lancet. 2006;368(9553):2110‐2111.

[3]. High Dose of Pralidoxime Reverses Paraoxon-Induced Respiratory Toxicity in Mice. Turk J Anaesthesiol Reanim. 2018;46(2):131‐138.

Pralidoxime is a pyridinium ion compound, a 1-methylpyridine compound in which a (hydroxyimino)methyl group is substituted at the 2-position. It is a cholinergic drug, a cholinesterase reactivator, an antidote for organophosphate poisoning, and an antidote for sarin poisoning. Pralidoxime is an antidote for organophosphate pesticides and chemicals. Organophosphates bind to the ester group of acetylcholinesterase, causing initial reversible inactivation of the enzyme. If taken within 24 hours of exposure to organophosphates, Pralidoxime can reactivate cholinesterase by cleaving the phosphate ester bond formed between the organophosphate and acetylcholinesterase. Pralidoxime is a cholinesterase reactivator. Pralidoxime's mechanism of action is as a cholinesterase reactivator. See also: Pralidoxime chloride (in salt form); Pralidoxime methyl sulfate (its active moiety). Drug Indications For the treatment of poisoning caused by organophosphate pesticides and chemicals with anticholinesterase activity, and for the control of overdose of anticholinesterase drugs used to treat myasthenia gravis. FDA Label Mechanism of Action Pralidoxime is an antidote for organophosphate pesticides and chemicals. Organophosphates bind to the esterification site of acetylcholinesterase, initially causing reversible inactivation of the enzyme. Inhibition of acetylcholinesterase leads to the accumulation of acetylcholine in the synapse, thereby continuously stimulating cholinergic fibers throughout the nervous system. If Pralidoxime is administered within 24 hours of exposure to organophosphates, it can reactivate acetylcholinesterase by cleaving the phosphate ester bond formed between the organophosphate and acetylcholinesterase. Other reported pharmacological effects of pralidoxime include neuromuscular junction depolarization, anticholinergic effects, mild cholinesterase inhibition, sympathomimetic effects, enhancement of the hypotensive effect of acetylcholine in atropine-free animals, and enhancement of the hypertensive effect of acetylcholine in atropine-injected animals. However, the contribution of these effects to the therapeutic effect of this drug has not been determined. The main pharmacological action of pralidoxime is the reactivation of cholinesterases that have been phosphorylated and inactivated by contact with certain organophosphates. Pralidoxime removes the phosphate group from the active site of the inhibited enzyme through nucleophilic attack, thereby restoring the activity of cholinesterase and forming an oxime complex. Pralidoxime can also detoxify certain organophosphates through direct chemical reactions and may also react directly with cholinesterase, protecting it from inhibition. Pralidoxime must be administered before the inhibited enzyme ages; after aging, phosphorylated cholinesterase cannot be reactivated and must be replaced by newly synthesized cholinesterase. Pralidoxime iodide's antagonistic effect on all anticholinesterases is not uniform, partly because the time required for the inhibited enzyme to age varies depending on the specific organophosphate that binds to the cholinesterase.

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Therapeutic Uses
Antidote; Cholinesterase Reactivator
/Clinical Trials/ ClinicalTrials.gov is a registry and results database that lists human clinical studies funded by public and private institutions worldwide. The website is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each record on ClinicalTrials.gov contains summary information about the study protocol, including: the disease or condition; the intervention (e.g., the medical product, behavior, or procedure being investigated); the title, description, and design of the study; participation requirements (eligibility criteria); the location of the study; contact information for the study location; and links to relevant information from other health websites, such as the NLM's MedlinePlus (which provides patient health information) and PubMed (which provides citations and abstracts of academic articles in the medical field). The antidote pralidoxime iodide is included in the database.
Protopam chloride can be used as an antidote: 1. For the treatment of poisoning caused by organophosphate pesticides and chemicals (such as nerve agents) with anticholinesterase activity; 2. For the control of anticholinesterase drug overdose used in the treatment of myasthenia gravis. The primary indications for protopam chloride are myasthenia gravis and respiratory depression. In cases of severe poisoning, respiratory depression may be due to myasthenia gravis. /Included on US product label/
Protopam chloride, used in combination with atropine, is used to treat nerve agent poisoning in the context of chemical warfare or terrorism. To ensure efficacy, protopam chloride must be taken within minutes to hours after exposure to the nerve agent. /Included on US product label/
For more complete data on the therapeutic uses of 2-PAMs (out of 8), please visit the HSDB record page.

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Drug Warning
Intramuscular injection of pralidoxime may cause mild pain at the injection site. Rapid intravenous injection of pralidoxime can cause tachycardia, laryngospasm, muscle stiffness, and transient neuromuscular blockade; therefore, this drug should be administered slowly, preferably via intravenous infusion. Intravenous pralidoxime has also been reported to cause hypertension, which is related to dosage and infusion rate. Some clinicians recommend monitoring patients' blood pressure during pralidoxime treatment. Intravenous administration of 5 mg phentolamine mesylate in adults has been reported to rapidly reverse pralidoxime-induced hypertension. Although pralidoxime is generally well tolerated, adverse reactions such as dizziness, blurred vision, diplopia and accommodation disorder, headache, drowsiness, nausea, tachycardia, hyperventilation, maculopapular rash, and muscle weakness have been reported. However, the toxicity of atropine or organophosphates is difficult to distinguish from that of pralidoxime, and the symptoms of organophosphate poisoning often mask the mild signs and symptoms observed in healthy subjects after taking pralidoxime. When atropine and pralidoxime are used concurrently, symptoms of atropine poisoning may appear earlier than when atropine is used alone, especially with a large total dose of atropine and delayed administration of pralidoxime. Agitation, confusion, manic behavior, and muscle rigidity have been reported after recovery of consciousness, but these symptoms have also appeared in patients not treated with pralidoxime. When treating anticholinesterase poisoning, the following precautions should be taken, although they are not directly related to the use of pralidoxime chloride: Barbiturates should be used with caution when treating seizures because their effects are enhanced by anticholinesterase; morphine, theophylline, aminophylline, reserpine, and phenothiazine sedatives should be avoided in patients with organophosphate poisoning. Succinylcholine has been reported to cause persistent paralysis when used in combination with drugs with anticholinesterase activity; therefore, caution should be exercised. For more complete data on drug warnings for 2-PAM (11 in total), please visit the HSDB records page.

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Pharmacodynamics
Pralidoxime can reactivate cholinesterase (primarily located outside the central nervous system) that has been inactivated by phosphorylation caused by organophosphorus pesticides or related compounds. This allows accumulated acetylcholine to be cleared, and the neuromuscular junction function to return to normal. Pralidoxime can also slow the process of phosphorylated cholinesterase "aging" into an inactivable form and detoxify certain organophosphorus compounds through direct chemical reactions. Its most important effect is relieving respiratory muscle paralysis. Because pralidoxime is less effective at relieving respiratory center depression, atropine is usually used concurrently to block the action of accumulated acetylcholine at that site. Pralidoxime can relieve muscarinic symptoms, salivation, bronchospasm, etc., but since atropine is sufficient to achieve this effect, this effect is relatively unimportant.

C7H9IN2O

264.07

263.975

94-63-3

Pralidoxime;6735-59-7

135398747

Light yellow to yellow solid powder

1.7439 g/ml

220 °C (dec.)(lit.)

1

2

1

10

125

0

C[N+]1=CC=CC=C1/C=N/O.[I-]

QNBVYCDYFJUNLO-UHFFFAOYSA-N

InChI=1S/C7H8N2O.HI/c1-9-5-3-2-4-7(9)6-8-10;/h2-6H,1H3;1H

(NE)-N-[(1-methylpyridin-1-ium-2-yl)methylidene]hydroxylamine;iodide

NSC 7760 NSC-7760 Pralidoxime iodide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

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

DMSO : ~250 mg/mL (~946.75 mM)

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.)