暴露于对氧磷引起的呼吸道毒性的小鼠可以通过单次肌肉注射碘解磷定（10-150 mg/kg）来恢复[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.

---

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.

---

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.

---

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.

---

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.

---

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.

---

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.)

36.47

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

注意： 请将本产品存放在密封且受保护的环境中（例如氮气保护），避免吸湿/受潮和光照。

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)

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

---

注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

View More

注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

---

口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

View More

口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

---

注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

---

请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。