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Pralidoxime iodide

Alias: NSC 7760 NSC-7760 Pralidoxime iodide
Cat No.:V14800 Purity: ≥98%
Pralidoxime iodideis an antidote for organophosphate poisoning, acting as areactivator of acetylcholinesterase (AChE).
Pralidoxime iodide
Pralidoxime iodide Chemical Structure CAS No.: 94-63-3
Product category: AChR Receptor
This product is for research use only, not for human use. We do not sell to patients.
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Other Forms of Pralidoxime iodide:

  • Pralidoxime
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Product Description

Description: Pralidoxime iodide is an antidote for organophosphate poisoning, acting as a reactivator of acetylcholinesterase (AChE). It acts by reactivating nerve agent-inhibited AChE via direct nucleophilic attack by the oxime moiety on the phosphorus center of the bound nerve agent. Pralidoxime is an antidote for organophosphate poisoning.

Biological Activity I Assay Protocols (From Reference)
ln Vivo
Mice exposed to respiratory toxicity caused by paraoxon can recover with a single intramuscular injection of pralidoxime iodide (10–150 mg/kg) [3].
Animal Protocol
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.
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
The drug is rapidly excreted in the urine partly unchanged, and partly as a metabolite produced by the liver.
It is not known if pralidoxime crosses the human placenta to the embryo or fetus. Pralidoxime chloride is a quaternary ammonium compound, but the molecular weight of the free base (about 137) is low enough for passage across the placenta. The rapid elimination of the drug should mitigate this transfer.
The specific mechanism by which the renal tubule handles pralidoxime, a quaternary ammonium compound used to reactivate organophosphate-inhibited cholinesterase, has been studied using 22 subjects. Each subject was placed under certain conditions in the course of the study. All 22 received pralidoxime (5 mg/kg, IV, over a 2-min interval) under conditions of forced hydration and bed rest to serve as controls. Eight subjects received pralidoxime under conditions of forced hydration and bed rest, one time after 36 hr of ammonium chloride acidification, and another time after sodium bicarbonate alkalinization. Nine subjects received pralidoxime under forced dehydration and bed rest, 20-30 min after thiamine (200 mg total, IM), organic base. Eight received pralidoxime under forced hydration and bed rest simultaneously with p-aminohippurate (900 mg total, IV), organic acid. Four received pralidoxime under bed rest, after 8-12 hr of fasting, NPO. The drug is rapidly cleared from the plasma by renal tubular secretion. Reduction of pralidoxime clearance rates and prolongation of the biologic half-life after thiamine administration as compared to those after PAH administration suggest that pralidoxime is secreted as an organic base. Reduction of the excretion of pralidoxime under conditions of both urine alkalinization and urine acidification implicates an active reabsorption of pralidoxime not heretofore described.
The pharmacokinetics of pralidoxime chloride (2-PAM) was studied in rats. Different groups of rats were given an intramuscular injection of 2-PAM at one of three doses (20, 40, or 80 mg/kg). This range of doses is used commonly in studies concerned with the efficacy of 2-PAM against poisoning by potent organophosphorus inhibitors of cholinesterase enzyme. Individual, sequential blood samples were collected during the course of the experiment. From these blood samples the plasma concentrations of 2-PAM were determined over time for each animal. Next the relationship of plasma concentration to time was expressed in terms of a standard pharmacokinetic model. Estimates of various pharmacokinetic parameters were calculated using an open, one-compartment model: volume of distribution (Vd), maximal plasma concentration (Cmax), elimination rate constant (k10), absorption rate constant (k01), area under the curve (AUC) and clearance (CL). Of the pharmacokinetic estimates, only Cmax and AUC were found to be statistically significant (p less than 0.0001) when compared across all the doses; these pharmacokinetic estimates were highly correlated with doses with r = 0.998 and r = 0.997, respectively. However, when AUC and Cmax were normalized by dividing through by dose, no significant differences were found in the transformed data. The results of this study in rat indicate that the pharmacokinetics of 2-PAM is linearly related to dose in a range employed in therapeutic studies of 2-PAM.
BACKGROUND: Current therapies for organophosphate poisoning involve administration of oximes, such as pralidoxime (2-PAM), that reactivate the enzyme acetylcholinesterase. Studies in animal models have shown a low concentration in the brain following systemic injection. METHODS: To assess 2-PAM transport, we studied transwell permeability in 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 for common brain efflux pumps, experiments were performed in the MDCKII-MDR1 cell line, transfected to overexpress the P-gp efflux pump, and the MDCKII-FLuc-ABCG2 cell line, transfected to overexpress the BCRP efflux pump. To determine how transcellular transport influences enzyme reactivation, we developed a modified transwell assay where the inhibited acetylcholinesterase enzyme, substrate, and reporter are introduced into the basolateral chamber. Enzymatic activity was inhibited using paraoxon and parathion. RESULTS: The permeability of 2-PAM is about 2 x 10(-6) cm/s in MDCK cells and about 1 x 10(-6) cm/s in BC1-hBMECs. Permeability is not influenced by pre-treatment with atropine. In addition, 2-PAM is not a substrate for the P-gp or BCRP efflux pumps. CONCLUSIONS: The low permeability explains poor brain penetration of 2-PAM and therefore the slow enzyme reactivation. This elucidates one of the reasons for the necessity of sustained intravascular (IV) infusion in response to organophosphate poisoning.
For more Absorption, Distribution and Excretion (Complete) data for 2-PAM (10 total), please visit the HSDB record page.
Metabolism / Metabolites
Hepatic
Although the exact metabolic fate of pralidoxime has not been completely elucidated, the drug is believed to be metabolized in the liver. ... A recent study has suggested that active tubular secretion may be involved, although the specific mechanism has not been identified.
There is a trend towards increasing doses of pralidoxime to treat human organophosphate poisonings that may have relevance in subpopulations. Indeed, pralidoxime is eliminated unchanged by the renal route. This study assesses the effect of renal failure on the kinetics of pralidoxime in a rat model of acute renal failure induced by potassium dichromate administration. On the first day, Sprague-Dawley rats received subcutaneously potassium dichromate (study) or saline (control). Forty-eight hours post-injection, animals received pralidoxime methylsulfate (50 mg/kg of pralidoxime base) intramuscularly. Blood specimens were sampled during 180 min after the injection. Urine was collected daily during the 3 days of the study. Plasma pralidoxime concentrations were measured by liquid chromatography with electrochemical detection. There was a 2-fold increase in mean elimination half-life and a 2.5-fold increase in mean area under the curve in the study compared to the control group. The mean total body clearance was halved in the study compared to the control group. Our study showed acute renal failure does not modify the distribution of pralidoxime but significantly alters its elimination from plasma. These results suggest that dosages of pralidoxime should be adjusted in organophosphate-poisoned humans with renal failure when using high dosage regimen of pralidoxime.
Biological Half-Life
74-77 minutes
The half-life of pralidoxime in patients with normal renal function varies and has been reported to range from 0.8-2.7 hours.
Toxicity/Toxicokinetics
Toxicity Summary
IDENTIFICATION AND USE: Pralidoxime is an antidote and cholinesterase reactivator used in the treatment of poisoning due to pesticides and chemicals which have anticholinesterase activity. It is also used to treatment overdoses by anticholinesterase drugs used in the treatment of myasthenia gravis. Pralidoxime chloride is used concomitantly with atropine for the treatment of nerve agent poisoning in the context of chemical warfare or terrorism. Pralidoxime chloride must be administered within minutes to hours following exposure to nerve agents to be effective. HUMAN STUDIES: Manifestations of overdosage in normal subjects include dizziness, blurred vision, diplopia, headache, impaired accommodation, nausea, and slight tachycardia. In therapy, it has been difficult to differentiate side effects due to the drug from those due to the effects of the poison. When atropine and pralidoxime chloride are used together, the signs of atropinization (flushing, mydriasis, tachycardia, dryness of the mouth and nose) may occur earlier than might be expected when atropine is used alone. ANIMAL STUDIES: Pralidoxime, used in the treatment of organophosphate poisoning, significantly increased cardiac output at all doses in open chest anesthetized dogs. A similar response was obtained in alpha-adrenergic blocked animals, but not with beta-adrenergic blocked or reserpine treated animals. All doses of pralidoxime significantly increased mean arterial pressure in control, beta-adrenergic blocked, and alpha-adrenergic blocked animals. Pralidoxime at 20 and 40 mg/kg also increased arterial pressure in reserpine treated animals. Heart rate was decreased in all but the alpha-adrenergic blocked animals with pralidoxime. The total peripheral resistance of the beta-blocked animals increased with every subsequent dose of pralidoxime although no significant increase was observed in controls. A smaller increase in total peripheral resistance was observed in reserpine-treated and alpha-adrenergic blocked animals. Significant increases in stroke volume and changes in stroke work were noted with all animals, each occurring at different atrial pressures depending on the treatment. The results suggest that pralidoxime directly stimulates the heart and vascular smooth muscle. Pralidoxime in dogs at high dosages, causes signs associated with its own anticholinesterase activity. Clinical signs of toxicity in dogs may be exhibited as muscle weakness, ataxia, vomiting, hyperventilation, seizures, respiratory arrest, and death.
Protein Binding
No binding to plasma proteins
Interactions
The pharmacokinetics of 5 mg/kg IV pralidoxime chloride (Protopam; I) when administered one hr after continuous infusion of thiamine hydrochloride (II) are described in 6 males. Subjects were given I alone and while receiving an infusion of II. After the addition of II, the urinary excretion of oxime was the same but the amount excreted in the first 3 hr was smaller; the plasma half-life of oxime lengthened; the plasma concentrations of oxime rose; and the intercompartmental clearances and rate constant for elimination for oxime fell. It was concluded that II and oxime compete for a common renal secretory mechanism or that II alters the membrane transport of oxime.
BACKGROUND AND PURPOSE: Treatment of organophosphate poisoning with pralidoxime needs to be improved. Here we have studied the pharmacokinetics of pralidoxime after its intramuscular injection alone or in combination with avizafone and atropine using an auto-injector device. EXPERIMENTAL APPROACH: The study was conducted in an open, randomized, single-dose, two-way, cross-over design. At each period, each subject received either intramuscular injections of pralidoxime (700 mg), or two injections of the combination: pralidoxime (350 mg), atropine (2 mg), avizafone (20 mg). Pralidoxime concentrations were quantified using a validated LC/MS-MS method. Two approaches were used to analyse these data: (i) a non-compartmental approach; and (ii) a compartmental modelling approach. KEY RESULTS: The injection of pralidoxime combination with atropine and avizafone provided a higher pralidoxime maximal concentration than that obtained after the injection of pralidoxime alone (out of bioequivalence range), while pralidoxime AUC values were equivalent. Pralidoxime concentrations reached their maximal value earlier after the injection of the combination. According to Akaike and to goodness of fit criteria, the best model describing the pharmacokinetics of pralidoxime was a two-compartment with a zero-order absorption model. When avizafone and atropine were injected with pralidoxime, the best model describing pralidoxime pharmacokinetics becomes a two-compartment with a first-order absorption model. CONCLUSIONS AND IMPLICATIONS: The two approaches, non-compartmental and compartmental, showed that the administration of avizafone and atropine with pralidoxime results in a faster absorption into the general circulation and higher maximal concentrations, compared with the administration of pralidoxime alone.
We have recently shown that the pyridinium aldoximes, best-known as therapeutic antidotes for chemical warfare nerve-agents, could markedly detoxify the carcinogenic tetrachloro-1,4-benzoquinone (TCBQ) via an unusual double Beckmann fragmentation mechanism. However, it is still not clear why pralidoxime (2-PAM) cannot provide full protection against TCBQ-induced biological damages even when 2-PAM was in excess. Here we show, unexpectedly, that TCBQ can also activate pralidoxime to generate a reactive iminyl radical intermediate in two-consecutive steps, which was detected and unequivocally characterized by the complementary application of ESR spin-trapping, HPLC/MS and nitrogen-15 isotope-labeling studies. The same iminyl radical was observed when TCBQ was substituted by other halogenated quinones. The end product of iminyl radical was isolated and identified as its corresponding reactive and toxic aldehyde. Based on these data, we proposed that the reaction of 2-PAM and TCBQ might be through the following two competing pathways: a nucleophilic attack of 2-PAM on TCBQ forms an unstable transient intermediate, which can decompose not only heterolytically to form 2-CMP via double Beckmann fragmentation, but also homolytically leading to the formation of a reactive iminyl radical in double-steps, which then via H abstraction and further hydrolyzation to form its corresponding more toxic aldehyde. Analogous radical homolysis mechanism was observed with other halogenated quinones and pyridinium aldoximes. This study represents the first detection and identification of reactive iminyl radical intermediates produced under normal physiological conditions, which provides direct experimental evidence to explain only the partial protection by 2-PAM against TCBQ-induced biological damages, and also the potential side-toxic effects induced by 2-PAM and other pyridinium aldoxime nerve-agent antidotes.
When atropine and pralidoxime chloride are used together, the signs of atropinization (flushing, mydriasis, tachycardia, dryness of the mouth and nose) may occur earlier than might be expected when atropine is used alone. This is especially true if the total dose of atropine has been large and the administration of pralidoxime chloride has been delayed.
The following precautions should be kept in mind in the treatment of anticholinesterase poisoning, although they do not bear directly on the use of pralidoxime chloride: since barbiturates are potentiated by the anticholinesterases, they should be used cautiously in the treatment of convulsions; morphine, theophylline, aminophylline, reserpine, and phenothiazine-type tranquilizers should be avoided in patients with organophosphate poisoning. Prolonged paralysis has been reported in patients when succinylcholine is given with drugs having anticholinesterase activity; therefore, it should be used with caution.
Non-Human Toxicity Values
LD50 Dog oral 190 mg/kg
References

[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.

Additional Infomation
Pralidoxime is a pyridinium ion that is 1-methylpyridinium substituted by a (hydroxyimino)methyl group at position 2. It has a role as a cholinergic drug, a cholinesterase reactivator, an antidote to organophosphate poisoning and an antidote to sarin poisoning.
Pralidoxime is an antidote to organophosphate pesticides and chemicals. Organophosphates bind to the esteratic site of acetylcholinesterase, which results initially in reversible inactivation of the enzyme. If given within 24 hours,after organophosphate exposure, pralidoxime reactivates the enzyme cholinesterase by cleaving the phosphate-ester bond formed between the organophosphate and acetylcholinesterase.
Pralidoxime is a Cholinesterase Reactivator. The mechanism of action of pralidoxime is as a Cholinesterase Reactivator.
See also: Pralidoxime Chloride (has salt form); Pralidoxime methyl sulfate (is active moiety of).
Drug Indication
For the treatment of poisoning due to those pesticides and chemicals of the organophosphate class which have anticholinesterase activity and in the control of overdosage by anticholinesterase drugs used in the treatment of myasthenia gravis.
FDA Label
Mechanism of Action
Pralidoxime is an antidote to organophosphate pesticides and chemicals. Organophosphates bind to the esteratic site of acetylcholinesterase, which results initially in reversible inactivation of the enzyme. Acetylcholinesterase inhibition causes acetylcholine to accumulate in synapses, producing continuous stimulation of cholinergic fibers throughout the nervous systems. If given within 24 hours after organophosphate exposure, pralidoxime reactivates the acetylcholinesterase by cleaving the phosphate-ester bond formed between the organophosphate and acetylcholinesterase.
Other reported pharmacologic effects of pralidoxime include depolarization at the neuromuscular junction, anticholinergic action, mild inhibition of cholinesterase, sympathomimetic effects, potentiation of the depressor action of acetylcholine in nonatropinized animals, and potentiation of the pressor action of acetylcholine in atropinized animals. However, the contribution of these effects to the therapeutic action of the drug has not been established.
The principal pharmacologic effect of pralidoxime is reactivation of cholinesterase which has been recently inactivated by phosphorylation as the result of exposure to certain organophosphates. Pralidoxime removes the phosphoryl group from the active site of the inhibited enzyme by nucleophilic attack, regenerating active cholinesterase and forming an oxime complex. Pralidoxime also detoxifies certain organophosphates by direct chemical reaction and probably also reacts directly with cholinesterase to protect it from inhibition. Pralidoxime must be administered before aging of the inhibited enzyme occurs; after aging is completed, phosphorylated cholinesterase cannot be reactivated, and newly synthesized cholinesterase must replace the inhibited enzyme. Pralidoxime is not equally antagonistic to all anticholinesterases, partly because the time period required for aging of the inhibited enzyme varies and depends on the specific organophosphate bound to the cholinesterase.
Therapeutic Uses
Antidotes; Cholinesterase Reactivators
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Pralidoxime is included in the database.
Protopam chloride is indicated as an antidote: 1. In the treatment of poisoning due to those pesticides and chemicals (e.g., nerve agents) of the organophosphate class which have anticholinesterase activity and 2. In the control of overdosage by anticholinesterase drugs used in the treatment of myasthenia gravis. The principal indications for the use of Protopam chloride are muscle weakness and respiratory depression. In severe poisoning, respiratory depression may be due to muscle weakness. /Included in US product label/
Pralidoxime chloride is used concomitantly with atropine for the treatment of nerve agent poisoning in the context of chemical warfare or terrorism. Pralidoxime chloride must be administered within minutes to hours following exposure to nerve agents to be effective. /Included in US product label/
For more Therapeutic Uses (Complete) data for 2-PAM (8 total), please visit the HSDB record page.
Drug Warnings
IM administration of pralidoxime may produce mild pain at the injection site.
Rapid IV injection of pralidoxime has produced tachycardia, laryngospasm, muscle rigidity, and transient neuromuscular blockade; therefore, the drug should be administered slowly, preferably by IV infusion. IV administration of pralidoxime reportedly may also cause hypertension which is related to the dose and rate of infusion. Some clinicians recommend that the patient's blood pressure be monitored during pralidoxime therapy. For adults, IV administration of 5 mg of phentolamine mesylate reportedly quickly reverses pralidoxime-induced hypertension.
Although pralidoxime is generally well-tolerated, dizziness, blurred vision, diplopia and impaired accommodation, headache, drowsiness, nausea, tachycardia, hyperventilation, maculopapular rash, and muscular weakness have been reported following administration of the drug. However, it is difficult to differentiate the toxic effects produced by atropine or organophosphates from those of pralidoxime, and the condition of patients suffering from organophosphate intoxication will generally mask minor signs and symptoms reported in normal subjects who receive pralidoxime. When atropine and pralidoxime are used concomitantly, signs of atropinism may occur earlier than when atropine is used alone, especially if the total dose of atropine is large and administration of pralidoxime is delayed. Excitement, confusion, manic behavior, and muscle rigidity have been reported following recovery of consciousness, but these symptoms have also occurred in patients who were not treated with pralidoxime.
The following precautions should be kept in mind in the treatment of anticholinesterase poisoning, although they do not bear directly on the use of pralidoxime chloride: since barbiturates are potentiated by the anticholinesterases, they should be used cautiously in the treatment of convulsions; morphine, theophylline, aminophylline, reserpine, and phenothiazine-type tranquilizers should be avoided in patients with organophosphate poisoning. Prolonged paralysis has been reported in patients when succinylcholine is given with drugs having anticholinesterase activity; therefore, it should be used with caution.
For more Drug Warnings (Complete) data for 2-PAM (11 total), please visit the HSDB record page.
Pharmacodynamics
Pralidoxime is to reactivate cholinesterase (mainly outside of the central nervous system) which has been inactivated by phosphorylation due to an organophosphate pesticide or related compound. The destruction of accumulated acetylcholine can then proceed, and neuromuscular junctions will again function normally. Pralidoxime also slows the process of "aging" of phosphorylated cholinesterase to a nonreactivatable form, and detoxifies certain organophosphates by direct chemical reaction. The drug has its most critical effect in relieving paralysis of the muscles of respiration. Because pralidoxime is less effective in relieving depression of the respiratory center, atropine is always required concomitantly to block the effect of accumulated acetylcholine at this site. Pralidoxime relieves muscarinic signs and symptoms, salivation, bronchospasm, etc., but this action is relatively unimportant since atropine is adequate for this purpose.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C7H9IN2O
Molecular Weight
264.07
Exact Mass
263.975
CAS #
94-63-3
Related CAS #
Pralidoxime;6735-59-7
PubChem CID
135398747
Appearance
Light yellow to yellow solid powder
Density
1.7439 g/ml
Melting Point
220 °C (dec.)(lit.)
Hydrogen Bond Donor Count
1
Hydrogen Bond Acceptor Count
2
Rotatable Bond Count
1
Heavy Atom Count
10
Complexity
125
Defined Atom Stereocenter Count
0
SMILES
C[N+]1=CC=CC=C1/C=N/O.[I-]
InChi Key
QNBVYCDYFJUNLO-UHFFFAOYSA-N
InChi Code
InChI=1S/C7H8N2O.HI/c1-9-5-3-2-4-7(9)6-8-10;/h2-6H,1H3;1H
Chemical Name
(NE)-N-[(1-methylpyridin-1-ium-2-yl)methylidene]hydroxylamine;iodide
Synonyms
NSC 7760 NSC-7760 Pralidoxime iodide
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

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.
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 : ~250 mg/mL (~946.75 mM)
Solubility (In Vivo)
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.

Injection Formulations
(e.g. IP/IV/IM/SC)
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 : PEG300Tween 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 : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH 400 μLPEG300 50 μL Tween 80 450 μL Saline)


Oral Formulations
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


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.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 3.7869 mL 18.9344 mL 37.8687 mL
5 mM 0.7574 mL 3.7869 mL 7.5737 mL
10 mM 0.3787 mL 1.8934 mL 3.7869 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.

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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.
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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.)
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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.

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