Absorption, Distribution and Excretion
Sevoflurane is rapidly absorbed into the bloodstream via the lungs; however, its solubility in blood is low (blood-gas partition coefficient of 0.63 to 0.69 at 37°C). Therefore, only a very small amount of sevoflurane dissolved in the blood is needed to induce anesthesia.
The low solubility of sevoflurane allows for rapid excretion via the lungs, with 95% to 98% of the anesthetic being cleared from the lungs.
Up to 3.5% of the sevoflurane dose appears in the urine as inorganic fluoride, and up to 50% of the fluoride is cleared via non-renal routes (fluoride is absorbed by the bones).
The peripheral distribution volume (n=16) of patients undergoing maxillofacial surgery under low-flow sevoflurane anesthesia was 1634 ml_vapor/kgbody weight, and the total distribution volume was 1748 ml_vapor/kgbody weight.
In patients (n=16) undergoing maxillofacial surgery under low-flow sevoflurane anesthesia, the transport clearance rate from the central ventricle to the peripheral ventricle was 13.0 ml_vapor/kg_{body weight}·min.
Up to 3.5% of the sevoflurane dose appears in the urine as inorganic fluoride. Fluoride studies have shown that up to 50% of fluoride clearance is not via the renal route (but via bone resorption).
The low solubility of sevoflurane allows for rapid pulmonary clearance. The clearance rate is quantified as the rate of change in alveolar (end-tidal) concentration (FA) after anesthesia termination relative to the final alveolar concentration (FaO) measured immediately before anesthesia termination.
Fluoride ion concentration is affected by the duration of anesthesia, the concentration of sevoflurane administered, and the composition of the anesthetic gas mixture. In studies using sevoflurane alone to maintain anesthesia for 1 to 6 hours, peak fluoride concentrations ranged from 12 μM to 90 μM. Peak concentrations are reached within 2 hours after anesthesia, and after 10 hours, plasma concentrations in most individuals are below 25 μM (475 ng/mL).
24 hours after anesthesia, sevoflurane concentrations in milk are likely not clinically significant. Due to its rapid clearance, sevoflurane concentrations in milk are expected to be lower than many other volatile anesthetics.
Compared to healthy individuals, patients with renal insufficiency have a prolonged fluoride half-life, but no prolonged fluoride half-life was observed in elderly patients. A study of 8 patients with hepatic impairment showed a slightly prolonged fluoride half-life. The mean half-life in patients with renal insufficiency is approximately 33 hours (range 21–61 hours), while the mean half-life in normal healthy individuals is approximately 21 hours (range 10–48 hours). The mean half-life in elderly individuals (over 65 years of age) is approximately 24 hours (range 18–72 hours). The mean half-life in individuals with impaired hepatic function is 23 hours (range 16–47 hours).

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Metabolism/Metabolites
Sevoflurane is metabolized to hexafluoroisopropanol via cytochrome P450 2E1, a reaction that promotes the release of inorganic fluorides and carbon dioxide. Hexafluoroisopropanol rapidly conjugates with glucuronic acid and is excreted in the urine. In vivo metabolic studies suggest that approximately 5% of the sevoflurane dose may be metabolized. In most cases, inorganic fluorides reach peak concentrations within 2 hours after the end of sevoflurane anesthesia and return to baseline levels within 48 hours. Sevoflurane metabolism may be induced by prolonged exposure to isoniazid and ethanol, while barbiturates do not affect its metabolism.
The nephrotoxicity and hepatotoxicity of fluorinated ether volatile anesthetics are due to their bioconversion into toxic metabolites. Metabolism also significantly affects the elimination pharmacokinetics of some volatile anesthetics. Although numerous studies have investigated the metabolism of anesthetics in animals, little information is available regarding the relative rates of metabolism of volatile anesthetics in humans or the types of enzymes responsible for defluorination. The primary objective of this study was to compare the metabolism of fluorinated ether anesthetics by human liver microsomes. Secondly, this study aimed to verify whether cytochrome P450 2E1 is a specific P450 isoenzyme responsible for the defluorination of volatile anesthetics in humans. Microsomes were obtained from human livers. The metabolism of anesthetics was assessed by measuring the amount of fluoride produced in the microsomal incubation solution. The strategy for assessing the role of P450 2E1 in anesthetic defluorination included three methods: analysis of 12 human liver tissue samples to determine the correlation between microsomal defluorination rate and microsomal P450 2E1 content (determined by Western blot analysis); determination of the correlation between defluorination rate and microsomal P450 2E1 catalytic activity using labeled substrates (hydroxylation of p-nitrophenol and 6-hydroxylation of chlorzoxazone); and chemical inhibition using selective inhibitors of P450 isoenzymes. The metabolic order of anesthetics, assessed by fluoride production at saturated substrate concentrations, was: methoxyflurane > sevoflurane > enflurane > isoflurane > desflurane > 0. Defluorination of sevoflurane and methoxyflurane showed a significant linear correlation with antigenic P450 2E1 levels (r = 0.98 and 0.72, respectively), but no correlation with P450 1A2 or P450 3A3/4. Comparison of anesthetic defluorination with the hydroxylation of p-nitrophenol or chlorzoxazone showed significant correlations for both sevoflurane (r = 0.93, r = 0.95) and methoxyflurane (r = 0.78, r = 0.66). Defluorination of sevoflurane was highly correlated with defluorination of enflurane (r = 0.93), which is known to be metabolized by human P450 2E1. Diethyldithiocarbamate is a selective inhibitor of P450 2E1, inhibiting the defluorination of sevoflurane, methoxyflurane, and isoflurane in a concentration-dependent manner. Other isoenzyme-selective inhibitors did not reduce the defluorination of sevoflurane, while the defluorination of methoxyflurane could be inhibited by the selective P450 inhibitors furazolidone (P450 1A2), sulfadiazine (P450 2C9/10), and quinidine (P450 2D6), but to a much lesser extent than diethyldithiocarbamate. These results indicate that cytochrome P450 2E1 is the major, and possibly only, enzyme catalyzing the defluorination of sevoflurane in human liver microsomes. P450 2E1 is the major enzyme in methoxyflurane metabolism, but not the only one; methoxyflurane metabolism also appears to be catalyzed by P450 1A2, 2C9/10, and 2D6. The data also suggest that P450 2E1 is responsible for a significant portion of isoflurane metabolism. Identifying P450 2E1 as the primary anesthetic metabolic enzyme in humans contributes to a mechanistic understanding of the metabolism and toxicity of clinically used fluoroether anesthetics. Sevoflurane (USP) is metabolized to hexafluoroisopropanol (HFIP), releasing inorganic fluorides and carbon dioxide. Fluoride ion concentration is affected by the duration of anesthesia and the concentration of sevoflurane (USP). After HFIP is generated, it rapidly conjugates with glucuronic acid and is excreted as a urinary metabolite. No other metabolic pathways for sevoflurane (USP) have been identified. In humans, the fluoride ion half-life is prolonged in patients with renal insufficiency, but no toxicity reports related to elevated fluoride ion levels have been observed in human clinical trials. Cytochrome P450 2E1 is the primary isoenzyme for sevoflurane metabolism, and its expression can be induced by prolonged exposure to isoniazid and ethanol. This is similar to the metabolism of isoflurane and enflurane, but different from the metabolism of methoxyflurane, which is metabolized by multiple cytochrome P450 isoenzymes. Barbiturates do not induce the metabolism of sevoflurane. As shown in Figure 5, in most cases (67%), inorganic fluoride concentrations peaked within 2 hours after sevoflurane anesthesia and returned to baseline levels within 48 hours post-anesthesia. Sevoflurane is rapidly and extensively cleared from the lungs, minimizing the amount of anesthetic dose available for metabolism. Sevoflurane is metabolized by cytochrome P450 2E1 to hexafluoroisopropanol (HFIP), releasing inorganic fluoride and carbon dioxide. HFIP is rapidly conjugated with glucuronic acid after formation and excreted as a urinary metabolite. No other metabolic pathways for sevoflurane have been identified. In vivo metabolic studies suggest that approximately 5% of the sevoflurane dose may be metabolized. In one study, four dogs exposed to 4% sevoflurane (USP) for 3 hours showed peak serum fluoride concentrations of 17.0–27.0 μmol/L 3 hours after anesthesia. Serum fluoride concentrations decreased rapidly after anesthesia and returned to baseline levels within 24 hours post-anesthesia.
Sepflurane undergoes relatively little biotransformation; only 5% is metabolized to hexafluoroisopropanol (HFIP) via cytochrome P450 CYP2E1, releasing inorganic fluoride and carbon dioxide. No other metabolic pathways for sevoflurane have been identified.
Elimination pathway: Sevoflurane's low solubility facilitates rapid elimination through the lungs. In vivo metabolic studies suggest that approximately 5% of the sevoflurane dose may be metabolized. Up to 3.5% of the sevoflurane dose appears in the urine as inorganic fluoride.
Half-life: 15–23 hours
Biological half-life
The elimination half-life of sevoflurane from the terminal peripheral fat compartment is approximately 20 hours.
Compared to healthy individuals, the fluoride half-life is prolonged in patients with renal insufficiency, but no prolonged fluoride half-life was observed in elderly patients. A study of eight patients with hepatic insufficiency showed a slightly prolonged sevoflurane half-life. The average half-life in patients with renal insufficiency is approximately 33 hours (range 21–61 hours), while the average half-life in healthy individuals is approximately 21 hours (range 10–48 hours). The average half-life in older adults (65 years and older) is approximately 24 hours (range 18–72 hours). The average half-life in individuals with impaired liver function is 23 hours (range 16–47 hours). The average half-life ranges from 15 to 23 hours.

Hepatotoxicity
Prospective serial blood tests typically show a slight, transient increase in serum transaminase levels within 1 to 2 weeks after major surgery. However, ALT levels exceeding 10 times the upper limit of normal are extremely rare, indicating severe hepatotoxicity. Clinically, severe liver injury caused by sevoflurane is very rare, with only sporadic case reports. This injury is characterized by an acute increase in serum transaminase levels (5 to 50 times) and the appearance of jaundice within 2 to 21 days post-surgery. Alkaline phosphatase and gamma-glutamyl transferase levels are usually only slightly elevated. Jaundice usually precedes fever by one or two days and may be accompanied by rash and eosinophilia. Acute liver injury may be self-limiting and resolve within 4 to 8 weeks, but it can also be severe and accompanied by acute liver failure. An important risk factor is prior exposure to any halogenated anesthetics, especially a history of halothane hepatitis or unexplained fever and rash after anesthesia with such drugs. Differential diagnosis of acute liver injury following surgery and anesthesia can sometimes be difficult. Clinical presentations similar to sevoflurane-induced hepatitis can also be caused by shock or ischemia, sepsis, other specific drug-induced liver injury, and acute viral or herpes simplex hepatitis.
Probability Score: B (Highly probable cause of clinically apparent liver injury).

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Pregnancy and Lactation Effects
◉ Overview of Lactational Use
Experience reports on the use of sevoflurane during lactation are scarce. Because sevoflurane has a short serum half-life in the mother and is not expected to be absorbed by the infant, there is no waiting period or need to discard breast milk. Breastfeeding can be resumed once the mother has recovered sufficiently from general anesthesia to be able to breastfeed. If multiple anesthetic drugs were used during surgery, the recommendations for the drug most likely to cause problems during the procedure should be followed. General anesthesia for cesarean section with sevoflurane as a component may delay the onset of lactation. A study showed that breastfeeding before induction of general anesthesia reduced the need for sevoflurane and propofol compared to breastfeeding mothers who had stopped breastfeeding or non-breastfeeding women.
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on lactation and breast milk
A randomized study compared the effects of cesarean section versus normal vaginal delivery under general anesthesia, spinal anesthesia, or epidural anesthesia on serum prolactin and oxytocin levels and the time to lactation initiation. All patients were induced with general anesthesia using propofol 2 mg/kg and rocuronium bromide 0.6 mg/kg, followed by sevoflurane and rocuronium bromide 0.15 mg/kg as needed. After delivery, all patients received an intravenous infusion of 30 IU oxytocin in 1 L of normal saline, and 0.2 mg ergonovine if blood pressure was normal. Patients in the general anesthesia group received fentanyl 1–1.5 mcg/kg post-delivery. Patients in the general anesthesia group (n = 21) had higher postoperative prolactin levels and a longer mean time to lactation initiation (25 hours) than other groups (10.8–11.8 hours). In the vaginal delivery group without assisted vaginal delivery, postpartum oxytocin levels were higher than in the general anesthesia and spinal anesthesia groups. A retrospective study compared women undergoing elective cesarean sections at a Turkish hospital, with differences in postpartum outcomes between women receiving bupivacaine spinal anesthesia (n = 170) and those receiving general anesthesia (n = 78). General anesthesia was induced with propofol, maintained with sevoflurane, and administered with fentanyl postpartum. Breastfeeding rates were similar between the two groups at 1 hour and 24 hours postpartum. However, at 6 months postpartum, the breastfeeding rate was 67% in the general anesthesia group and 81% in the spinal anesthesia group, a statistically significant difference. Protein binding of sevoflurane has not been assessed. In vitro analyses have shown that other fluorinated volatile anesthetics can displace the drug from serum and tissue proteins; however, the clinical significance of this displacement remains unclear. Clinical studies have shown that sevoflurane does not have a significant effect on patients taking drugs with high binding rates and small volumes of distribution.

Sevoflurane is an ether compound with two alkyl groups: fluoromethyl and 1,1,1,3,3,3-hexafluoroisopropyl. It is used as an inhalation anesthetic, platelet aggregation inhibitor, and central nervous system depressant. It is an organofluorine compound and also an ether compound. Its structure is similar to 2-methoxypropane. Sevoflurane is an ether-based inhalation anesthetic used for induction and maintenance of general anesthesia. It is a volatile, non-flammable compound with low solubility and a low blood/gas partition coefficient. Sevoflurane was patented in 1972, approved for clinical use in Japan in 1990, and approved by the U.S. Food and Drug Administration (FDA) in 1996. Sevoflurane is three times more potent than desflurane, but less potent than halothane and isoflurane. Unlike other volatile anesthetics, sevoflurane has a pleasant odor and does not irritate the respiratory tract. The hemodynamic and respiratory depressant effects of sevoflurane are well-tolerated, and most patients receiving this anesthetic experience only mild toxicity. Therefore, it can be used for inhalation induction of various anesthetic procedures in adults and children.
Sevoflurane is a general anesthetic. Its physiological effects are achieved through general anesthesia.
Sevoflurane is one of the most commonly used volatile anesthetics, particularly suitable for outpatient anesthesia, and has an excellent safety profile. Rare case reports have associated sevoflurane with severe acute liver injury similar to halothane hepatitis.
Sevoflurane is a fluorinated isopropyl ether with general anesthetic effects. Although its mechanism of action is not fully elucidated, sevoflurane may exert its effects by interfering with the release and reuptake of neurotransmitters at postsynaptic terminals and/or altering ion conductance after neurotransmitter activation of receptors. Sevoflurane may also interact directly with the lipid matrix of neuronal membranes, thereby affecting the gating properties of ion channels. Furthermore, the drug may activate γ-aminobutyric acid (GABA) receptors, leading to cell membrane hyperpolarization. This results in general anesthesia, decreased myocardial contractility, decreased mean arterial pressure, and increased respiratory rate.
Sevoflurane is only present in individuals who have used or taken this drug. Sevoflurane (2,2,2-trifluoro-1-[trifluoromethyl]ethylfluoromethyl ether), also known as fluoromethyl, is a sweet-smelling, non-flammable, highly fluorinated methyl isopropyl ether used for the induction and maintenance of general anesthesia. Along with desflurane, it is replacing isoflurane and halothane in modern anesthesiology. [Wikipedia] Sevoflurane reduces junctional conductance by shortening the opening time and prolonging the closing time of gap junction channels. Sevoflurane can also activate calcium-dependent ATPases in the sarcoplasmic reticulum by increasing lipid membrane fluidity. It can also bind to the D subunit of ATP synthase and NADH dehydrogenase, and can bind to GABA receptors, high-conductivity Ca²⁺-activated potassium channels, glutamate receptors, and glycine receptors. It is a non-explosive inhaled anesthetic used for the induction and maintenance of general anesthesia. It does not cause airway irritation and may also inhibit platelet aggregation. Drug Indications: Sevoflurane is used for the induction and maintenance of general anesthesia in adult and pediatric inpatient and outpatient surgical patients.
Used for the induction and maintenance of anesthesia.
Used for the induction and maintenance of anesthesia in dogs and cats.

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Mechanism of Action
The exact mechanism of action of sevoflurane is not fully understood. Like other halogenated inhaled anesthetics, sevoflurane induces anesthesia by binding to ligand-gated ion channels and blocking neurotransmission in the central nervous system. Studies have shown that inhaled anesthetics enhance inhibitory postsynaptic channel activity by binding to GABA_A and glycine receptors, and inhibit excitatory synaptic channel activity by binding to nicotinic acetylcholine receptors, serotonin receptors, and glutamate receptors. Sevoflurane affects a variety of ion currents, including hyperpolarized activated cation current (I_f), T-type and L-type Ca²⁺ currents (I_Ca,T and I_Ca,L), slow-activated delayed rectified K₊ current (I_Ks), and Na⁺/Ca²⁺ exchange current (I_NCX). This ability to modulate ion channel activity also modulates cardiac excitability and contractility. Sevoflurane is widely used as a volatile anesthetic in clinical practice. However, its mechanism of action remains unclear. …It has been reported that voltage-gated sodium channels play an important role in the mechanism of anesthesia. The effects of sevoflurane on voltage-dependent sodium channels have attracted considerable attention. To clarify this, researchers examined the effects of sevoflurane on Nav1.8, Nav1.4, and Nav1.7 channels expressed in Xenopus laevis oocytes. Using a whole-cell two-electrode voltage-clamp technique, they investigated the effects of sevoflurane on these sodium channels in Xenopus laevis oocytes via electrophysiological methods. The results showed that 1.0 mM sevoflurane inhibited voltage-gated sodium channels Nav1.8, Nav1.4, and Nav1.7, while 0.5 mM sevoflurane had almost no effect. This inhibitory effect of 1 mM sevoflurane was completely eliminated by pretreatment with the protein kinase C (PKC) inhibitor bisindolylmaleimide I. Sevoflurane appears to inhibit Na(v)1.8, Na(v)1.4, and Na(v)1.7 channels via the PKC pathway. However, these sodium channels may not be relevant to the clinical anesthetic effects of sevoflurane. Sevoflurane has been shown to dilate placental vessels. Researchers aimed to determine the contribution of potassium and calcium channel function regulation to the vasodilatory effect of sevoflurane in isolated human chorionic arterial rings. All studies used four isolated human chorionic arterial rings. Series 1 and 2 investigated the role of K+ channels in sevoflurane-mediated vasodilation. Different experiments investigated whether tetraethylammonium (which blocks high-conductivity calcium-activated potassium channels (KCa++), Series 1A+B) or glibenclamide (which blocks ATP-sensitive potassium channels (KATP), Series 2) modulated sevoflurane-mediated vasodilation. Series 3–5 investigated the role of calcium channels in sevoflurane-induced vasodilation. Different experiments investigated whether verapamil (blocks voltage-gated calcium channels in the chorionic villus (Series 3), SK&F 96365 (inhibits voltage-independent calcium channels in the chorionic villus (Series 4A+B),) or rhinodin (inhibits sarcoplasmic reticulum calcium channels (Series 5A+B)) modulates sevoflurane-mediated vasodilation. In all studies, sevoflurane dose-dependently dilated the chorionic villus arterial ring. Pre-blocking of KCa++ and KATP channels enhanced the vasodilatory effect of sevoflurane. Furthermore, pretreatment of the arterial ring with sevoflurane before administration of TEA blocked the effect of TEA. In summary, these results indicate that sevoflurane blocks K+ channels. Blocking voltage-gated Ca++ channels inhibits the vasodilatory effect of sevoflurane. Conversely, blocking voltage-independent Ca++ channels and sarcoplasmic reticulum Ca++ channels did not affect the vasodilatory effect of sevoflurane. Sevoflurane appears to block KCa++ and KATP channels in the chorionic villus arteries. Sevoflurane also blocks voltage-gated calcium channels and exerts net vasodilatory effects in in vitro placental circulation. Administration of sevoflurane at the start of reperfusion has been shown to provide neuroprotection; however, the mechanism remains unclear. This study aimed to verify whether sevoflurane posttreatment induces neuroprotection by upregulating hypoxia-inducible factor-1α (HIF-1α) and heme oxygenase-1 (HO-1), a process involving the phosphatidylinositol-3-kinase (PI3K)/Akt pathway. In the first experiment, male Sprague-Dawley rats underwent focal cerebral ischemia. Posttreatment with 2.5% sevoflurane was administered immediately at the start of reperfusion. At 6, 24, and 72 hours post-reperfusion, the mRNA and protein expression of HIF-1α and its target gene HO-1, intact neurons, and caspase-3 activity were assessed. In the second experiment, the relationship between the PI3K/Akt pathway and the expression of HIF-1α and HO-1 in the sevoflurane-induced neuroprotective effect was investigated. At 24 hours post-reperfusion, infarct volume, apoptotic neurons, and the expression of HIF-1α, HO-1, and p-Akt were assessed. Compared with the control group, sevoflurane posttreatment significantly reduced neuronal damage, upregulated the mRNA and protein levels of HIF-1α and HO-1, inhibited caspase-3 activity, and reduced the number of TUNEL-positive cells and infarct area. However, the selective PI3K inhibitor wollamine not only partially eliminated the neuroprotective effect of sevoflurane (manifested as a reduction in infarct area and the number of apoptotic neurons), but also reversed the sevoflurane-induced increase in the expression of HIF-1α, HO-1, and p-Akt in the ischemic penumbra. Therefore, these data suggest that the neuroprotective effect of sevoflurane posttreatment is partly mediated by the upregulation of HIF-1α and HO-1 through the PI3K/Akt pathway. Sevoflurane is widely used in anesthesia and is often used in combination with opioids in clinical practice. However, the effect of sevoflurane on μ-opioid receptor (μOR) function remains unclear. This study analyzed the effect of sevoflurane on uOR function using Xenopus laevis oocytes expressing uOR fused with chimeric Gα protein G(qi5) (uOR-G(qi5)). Sevoflurane itself does not induce any current in oocytes expressing uOR-G(qi5), but at clinically common concentrations, sevoflurane inhibits the [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO)-induced Cl⁻ current. Sevoflurane does not affect AlF₄⁻-induced Cl⁻ current, while AlF₄⁻ can directly activate G proteins. In oocytes pretreated with the protein kinase C (PKC) inhibitor GF109203X, no inhibitory effect of sevoflurane on DAMGO-induced current was observed. These findings indicate that sevoflurane inhibits uOR function. Furthermore, the inhibitory mechanism of sevoflurane may be mediated by PKC. For more data (9 items in total) on the complete mechanism of action of sevoflurane, please visit the HSDB record page.

200.0548

200.007

28523-86-6

5206

Liquid

1.4±0.1 g/cm3

49.5±35.0 °C at 760 mmHg

50-60ºC

-11.4±21.8 °C

311.5±0.1 mmHg at 25°C

1.266

2.48

0

8

2

12

121

0

FC(C([H])(C(F)(F)F)OC([H])([H])F)(F)F

DFEYYRMXOJXZRJ-UHFFFAOYSA-N

InChI=1S/C4H3F7O/c5-1-12-2(3(6,7)8)4(9,10)11/h2H,1H2

1,1,1,3,3,3-hexafluoro-2-(fluoromethoxy)propane

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

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.)