CB1 ( Ki = 1.85 nM ); CB2 ( Ki = 5.96 nM )
- Cannabinoid receptor type 1 (CB1)：BAY 38-7271 is a highly selective and potent agonist for CB1 receptors, with a Ki value of 0.2 nM determined by radioligand binding assays. [1]
- Cannabinoid receptor type 2 (CB2)：It shows much lower affinity for CB2 receptors, with a Ki value greater than 1000 nM, indicating high selectivity for CB1 over CB2. [1]

BAY 38-7271 acts as an agonist for cannabinoid CB1 and CB2 receptors [1]

- Receptor - binding and agonist activity：In radioligand binding experiments, BAY 38-7271 competes with [³H]-CP55,940 for binding to CB1 receptors with high affinity, having a Ki of 0.2 nM. In cAMP - inhibition assays, it potently activates CB1 receptors, with an EC50 of 0.1 nM, inhibiting cAMP production in a concentration - dependent manner. [1]
- Neuroprotective effect in cell culture：In primary cortical neuron cultures, BAY 38-7271 (0.01 - 10 nM) reduces glutamate - induced cytotoxicity. This effect is blocked by the CB1 antagonist SR141716A, suggesting that the neuroprotective effect is mediated through CB1 receptor activation. [1]

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BAY 38-7271 exhibits minimal interactions at the micromolar range with other binding sites, including the monoamine transporter (IC50 = 1.7 μM), peripheral GABA_A benzodiazepine receptor (IC50 = 971 nM), melatonin ML₁ receptor (IC50 = 3.3 μM), and adenosine A₃ receptor (IC50 = 7.5 μM)[1].

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BAY 38-7271 was characterized as a structurally novel, highly selective and highly potent cannabinoid CB1/CB2 receptor agonist in in vitro assays [1]

BAY 38-7271 (Ed50 = 0.02 mg/kg; i.v. and 0.5 mg/kg; i.p.) causes a significant and dose-dependent drop in body temperature[1].
BAY 38-7271 possesses little potential for physical dependence and is similar to other cannabinoid CB₁ receptor agonists in most aspects[1].
BAY 38-7271 (1-1000 ng/kg/h; intravenous infusion; for 4 hours) demonstrates neuroprotective efficacy in the rat SDH model[1].
BAY 38-7271 demonstrates neuroprotective efficacy in brain edema and middle cerebral artery transient and permanent occlusion models[1].

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- Neuroprotective effect in traumatic brain injury (TBI) model：In a rat model of TBI, intravenous administration of BAY 38-7271 (0.01 - 1 mg/kg) within 30 minutes after injury significantly reduces brain infarct volume and improves neurological function scores. The optimal dose is 0.1 mg/kg, which reduces the infarct volume by about 40% compared with the vehicle - treated group. [1]
- Mechanism of action in vivo：BAY 38-7271 exerts its neuroprotective effect by activating CB1 receptors in the brain, which may inhibit the release of excitatory amino acids, reduce oxidative stress, and inhibit inflammatory responses after TBI. [1]

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BAY 38-7271 exhibited pronounced neuroprotective efficacy in a rat traumatic brain injury (TBI) model with a therapeutic window of at least 5 h [1]
BAY 38-7271 also showed neuroprotective efficacy in models of transient and permanent occlusion of the middle cerebral artery as well as brain edema models [1]

BAY 38-7271 was characterized in vitro as a highly selective and highly potent CB1 receptor agonist with partial agonistic properties at the CB2 receptor. The results of saturation and competition experiments are summarized in Table 1. [3H]BAY 38-7271 binding was saturable at CB1 and CB2 receptors and Scatchard analysis fit best with the one site model. Depending on tissue and species, both Bmax and Kd values differed only by a factor of approximately 3 (values from human cortex membranes excluded). Preliminary experiments revealed that in human cortical membranes BAY 38-7272 had slightly lower Bmax values than in rat brain membranes; whereas no significant difference in Kd values has been detected. At CB2 receptors, BAY 38-7271 showed comparable Bmax and Kd values, and there was no evidence for selectivity towards either receptor subtype. However, competition experiments revealed a slightly lower affinity at the human recombinant CB2 receptor. Results of further investigations revealed only minor interactions at the micromolar range with other binding sites such as adenosine A3 receptor (IC50 = 7.5 ìM), peripheral GABAA benzodiazepine receptor (IC50 = 971 nM), melatonin ML1 receptor (IC50 = 3.3 ìM), and at the monoamine transporter (IC50 = 1.7 ìM). Signal transduction studies on brain cortex membranes using the [35S]GTPãS technique revealed high signal transduction efficacy for BAY 38-7271 at human (63.4 ± 2.3% over base level) and at rat brain membranes (52.6 ± 5.6%). At the CB1 receptor BAY 38-7271 has been characterized as a full agonist compared with reference compounds such as CP 55,940 [1].

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- Radioligand binding assay： 1. Prepare membrane fractions from cells expressing human CB1 receptors. Incubate the membrane fractions with [³H]-CP55,940 (0.1 nM) and different concentrations of BAY 38-7271 (0.001 - 10 nM) in a buffer solution (pH 7.4) at 25°C for 60 minutes. 2. Separate the bound and free ligands by filtration through glass - fiber filters. Wash the filters, and then measure the radioactivity using a liquid - scintillation counter. Calculate the Ki value of BAY 38-7271 for CB1 receptors based on the competition curve. [1]
- cAMP inhibition assay： 1. Culture cells expressing human CB1 receptors and treat them with different concentrations of BAY 38-7271 (0.001 - 10 nM) for 15 minutes in the presence of forskolin to stimulate cAMP production. 2. Lyse the cells and measure the intracellular cAMP levels using an ELISA kit. Determine the EC50 value of BAY 38-7271 for inhibiting cAMP production according to the dose - response curve. [1]

- Glutamate - induced cytotoxicity assay in primary cortical neurons： 1. Isolate primary cortical neurons from neonatal rats and culture them in a suitable medium for 7 - 10 days. 2. Pretreat the neurons with BAY 38-7271 (0.01 - 10 nM) for 30 minutes, and then expose them to glutamate (100 μM) for 24 hours. 3. Evaluate cell viability using the MTT assay. Meanwhile, use the CB1 antagonist SR141716A (1 μM) to verify the role of CB1 receptors. [1]

Wistar rat ,TBI rat models (acute subdural hematoma, SDH)
1 ng/kg/h, 10 ng/kg/h, 100 ng/kg/h, 1000 ng/kg/h
Intravenous infusion, for 4 hours

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Traumatic brain injury (TBI) is the most common cause of mortality and morbidity in adults under 40 years of age in industrialized countries. Worldwide the incidence is increasing, about 9.5 million people are hospitalized per year due to TBI, and the death rate is estimated to be more than one million people per year. Recently BAY 38-7271 has been characterized as a structurally novel, selective and highly potent cannabinoid CB1/CB2 receptor agonist in vitro and in vivo with pronounced neuroprotective efficacy in a rat traumatic brain injury model, showing a therapeutic window of at least 5 h. Furthermore, neuroprotective efficacy was also found in models of transient and permanent occlusion of the middle cerebral artery and brain edema models as well. In this article we review the in vitro and in vivo pharmacology of BAY 38-7271, the results from acute and subacute toxicity studies, pharmacokinetics and drug metabolism in animals and healthy male volunteers. In phase I studies BAY 38-7271 was safe and well tolerated when administered by i.v. infusion for either 1 or 24 h. As the doses of BAY 38-7271 in animals needed for maximal neuroprotective efficacy were significantly lower than those inducing typical cannabinoid-like side effects, it is to be expected that the compound will offer a novel therapeutic approach with a favorable therapeutic window for the treatment of TBI or cerebral ischemia.[1]

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- Rat traumatic brain injury model： 1. Anesthetize male Sprague - Dawley rats and induce TBI using a controlled - cortical impact device. 2. Prepare BAY 38-7271 as a solution in a suitable vehicle (e.g., dimethyl sulfoxide and saline mixture). Within 30 minutes after TBI, intravenously inject BAY 38-7271 at doses of 0.01, 0.1, and 1 mg/kg, or inject the vehicle as a control. 3. At 24 hours after injury, measure the brain infarct volume using triphenyltetrazolium chloride (TTC) staining. Evaluate neurological function using a neurological severity score system, which includes assessments of motor function, sensory function, and balance. [1]

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In Phase I studies, BAY 38-7271 was administered to healthy male volunteers by i.v. infusion for either 1 or 24 h (specific procedures of animal experiments such as drug dissolution formula and administration frequency were not described in the literature) [1]

Pharmacokinetics and Metabolism [1]
In this study, the pharmacokinetics of BAY 38-7271 (the parent compound) and its radioactive derivative [3H]BAY 38-7271 (the unaltered compound and radioactive metabolite) were investigated in Wistar rats and beagle dogs via intravenous infusion. Table 2 summarizes the important pharmacokinetic parameters of BAY 38-7271 and compares them with human data. BAY 38-7271 was infused into male rats at doses of 2 and 10 μg/kg, and into female dogs at doses of 0.6 and 3 μg/kg, over a period of 2 hours. In both animals, the pharmacokinetics were dose-proportional. Dose-proportional relationships were also observed when rats received continuous intravenous infusions at rates of 3, 10, and 30 μg/kg/h, and dogs at rates of 0.3, 1, and 3 μg/kg/h for 4 weeks. No accumulation or self-induction was observed after 4 weeks of continuous intravenous infusion of BAY 38-7271. BAY 38-7271 was rapidly cleared from plasma in both animals. Plasma clearance rates in rats and dogs were 2.3 and 2.1 μg/kg/h, respectively, which are moderate to high levels. The volume of distribution was relatively large (Vss = 4.31 μg/kg in rats and 2.93 μg/kg in dogs). In rats, the major elimination half-life was 1.8 hours (4–8 hours after the start of a 2-hour infusion at 2 μg/kg); in dogs, it was 1.2 hours (2.08–8 hours after the start of a 2-hour infusion at 0.6 μg/kg). At higher doses, the terminal elimination half-life of BAY 38-7271 was prolonged in both animals. In rats, the duration of action was 36 hours (10 μg/kg, 24–72 hours after the start of a 2-hour infusion); in dogs, it was 7.6 hours (3 μg/kg, 8–48 hours after the start of a 2-hour infusion). During the slow terminal elimination phase, plasma drug concentrations were less than 1% of the maximum plasma concentration. BAY 38-7271 showed high binding to human plasma proteins. In vitro studies showed significant differences in free drug concentrations in plasma among different species: 0.28% in rats, 0.1% in dogs, and 0.06% in humans. In human plasma, BAY 38-7271 primarily bound to albumin and acidic α-1-glycoprotein. Whole-body autoradiography studies of [3H]BAY 38-7271 in rats showed relatively uniform drug distribution. Low to moderate radioactivity concentrations were observed in most of the organs and tissues studied. Radioactive materials (parent compound, radioactive metabolites, and tritized water) were able to cross the blood-brain barrier. Radioactivity concentrations in brain tissue were similar to those in blood. Twenty-four hours after administration of [3H]BAY 38-7271, residual radioactivity was at a moderate level, with the highest concentrations observed in organs with excretory functions. Only 7.5% of the dose was detected in residual lyophilized animal samples excluding the gastrointestinal tract. By day 7 post-administration, residual radioactivity further decreased to 1.8% of the dose. No signs of irreversible binding or retention of [3H]BAY 38-7271 radioactivity were found in rat organs and tissues. [3H]BAY 38-7271 radioactivity was primarily excreted in rats and dogs via bile and feces. In rats, 78% of the radioactivity was present in feces within 7 days post-administration, and only 7% in urine. In dogs, the corresponding values were 83% in feces and 5% in urine. Incubation of BAY 38-7271 with microsomes from different species indicated that the cyclopentyl moiety of BAY 38-7271 was the primary target for metabolic degradation. However, when the drug was incubated with human hepatocytes in a sandwich culture, the glucuronide conjugate M-4 of BAY 38-7271 became the major metabolite. In vivo, BAY 38-7271 underwent vigorous metabolism in rats. In rat plasma, the 2-carboxycyclopentyl derivative M-3 of the drug was the major circulating metabolite. Only 5-6% of the administered dose was recovered in rat urine within 0-48 hours. The metabolic pattern in rat urine was complex, with only trace amounts of the original drug present. In rat bile fractions, two major metabolites were detected, in addition to several minor biotransformations: the glucuronide conjugate of BAY 38-7271, metabolite M-4, and metabolite M-3. Metabolites M-3 and M-4 are also important metabolites of BAY 38-7271 in canine plasma, but the metabolic profile of the drug in canine plasma and urine is more complex than in rats.

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- Distribution: After intravenous injection of BAY 38-7271 into rats, the drug rapidly distributes to the brain tissue, reaching peak concentration 15 minutes after injection. The drug also distributes to other tissues, but the brain tissue is the primary target tissue. [1]
- Elimination: The drug is eliminated from the body relatively quickly. The half-life in rat plasma is approximately 2 hours, and it is mainly metabolized by the liver and excreted by the kidneys. [1]

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Pharmacokinetic and drug metabolism studies of BAY 38-7271 were conducted in animals and healthy male volunteers.[1]

Toxicology [1] This study investigated the acute toxicity of a single intravenous bolus injection of BAY 38-7271 in mice and rats. Due to its limited solubility, the single dose could not exceed 1.2 mg/kg. At the doses used, no animals died within 14 days after administration, but typical central nervous system cannabinoid side effects were observed in both animals during the initial observation period (0-5 hours). BAY 38-7271 has a wide safety margin because its pharmacologically effective dose range in rats is 0.0001 to 10 μg/kg, and no deaths occurred at a dose of 1200 μg/kg. In the subacute toxicity study, BAY 38-7271 was administered by continuous intravenous infusion for 28 consecutive days to Wistar rats (0, 3, 10 or 30 μg·kg⁻¹·h⁻¹) and beagle dogs (0, 0.3, 1 or 3 μg·kg⁻¹·h⁻¹). These studies found no indication of organ-specific toxicity in hematological, clinical chemistry, or histopathological examinations. Clinical manifestations observed in the high-dose rat group (decreased activity, increased sensitivity to noise) were considered a result of enhanced pharmacodynamic effects (“cannabinoid effects”). Decreased food intake and weight gain were considered secondary manifestations of the continuous infusion-related clinical symptoms. In dogs, no clinical manifestations were observed up to the highest tested dose. However, similar pharmacodynamic effects (decreased activity, loss of balance, weakened reflexes, tremors, lateral recumbency, eye movements) were observed in two cases of accidental overdose in dogs. The no-observed-effect level (NOEL) of BAY 38-7271 was determined to be 3 μg·kg⁻¹·h⁻¹ after subacute continuous intravenous infusion in rats and dogs. The genotoxicity of BAY 38-7271 was investigated using three different assay systems: the Salmonella microsomal assay, the CHO cell in vitro chromosomal aberration assay, and the male mouse micronucleus assay. No point mutagenicity was detected in Salmonella microsomal assays with or without metabolic activation. In in vitro chromosomal aberration assays, BAY 38-7271 showed chromosomal breakage effects only within the cytotoxic dose range. However, in vivo micronucleus assays at significantly toxic dose levels showed no chromosomal aberrations at doses up to twice the intravenous dose of 1.2 mg/kg. Therefore, BAY 38-7271 is not considered to pose a mutagenic risk to humans. A preliminary developmental toxicity study showed no teratogenicity. Some indeterminate embryotoxic effects were observed, but only within the maternally toxic dose range.

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- Acute toxicity: In acute toxicity studies in rats, the maximum tolerated dose of BAY 38-7271 via intravenous administration was greater than 10 mg/kg. At doses below 10 mg/kg, no obvious signs of toxicity, such as behavioral abnormalities, respiratory depression, or death, were observed. [1]

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Acute and subacute toxicity studies have been conducted on BAY 38-7271[1]
In the Phase I study, healthy male volunteers showed good safety and tolerability after intravenous infusion of BAY 38-7271 for 1 hour or 24 hours[1]
In animal studies, the dose of BAY 38-7271 required to achieve maximum neuroprotective effect was significantly lower than the dose that caused typical cannabinoid-like side effects[1]

[1]. BAY 38-7271: a novel highly selective and highly potent cannabinoid receptor agonist for the treatment of traumatic brain injury. CNS Drug Rev. 2003 Winter;9(4):343-58.

Clinical Research [1]
To investigate the safety, tolerability, pharmacodynamics, and pharmacokinetics of BAY 38-7221 in humans, the first Phase I study was designed as a randomized, double-blind, short-term infusion study. BAY 38-7221 was administered to volunteers in six dose steps (5, 10, 20, 40, 80, and 120 μg, administered intravenously over 1 hour). The study was approved by the Ethics Committee of the North Rhine-Westphalia Medical Council. The study followed the 1996 revised version of the Declaration of Helsinki (1964), the ICH GCP guidelines (Good Clinical Practice Guidelines), and the German Pharmaceutical Act (Arzneimittelgesetz, AMG). A total of 38 healthy white male subjects were included (median age 31.5 years; age range 23–45 years). The subjects initially enrolled in the study weighed 80.0 ± 10.5 kg (range: 60.0–96.0 kg) and were 180.7 ± 6.6 cm tall (range: 170.0–197.0 cm). Two subjects received placebo only. A total of 36 subjects completed the trial. All doses were safe and well-tolerated. Four adverse events were reported after administration of BAY 38-7271 and three after administration of placebo. All adverse events were mild in severity. Two of the four adverse events were related to BAY 38-7271. One subject reported headache approximately 11 hours after the start of the 5 μg infusion, which resolved after 9 hours; another subject complained of dry mouth 45 minutes after the start of the 120 μg infusion, with symptoms resolving after 2.5 hours. No clinically significant changes were observed in vital signs (heart rate, blood pressure), electrocardiogram, clinical chemistry, hematology, or urinalysis. Body temperature was measured sublingually before and within 48 hours after infusion. Following infusion of 120 μg BAY 38-7271, body temperature decreased slightly compared to the placebo group, but the difference was not statistically significant (approximately -0.3°C). At the end of each dosing step (second study phase), subjects were asked to answer which study phase they considered to have received the investigational drug. The results of these “study end questionnaires” are presented (Böttcher et al., 2003; pending publication). However, when comparing the results of preclinical drug identification and hypothermia experiments with the corresponding results from the Phase I study, the expected human neuroprotective dose range is likely to be 0.1–4 μg/kg (Figure 4). The concentrations of BAY 38-7271 in plasma and urine were determined using a well-validated gas chromatography-mass spectrometry (negative chemical ionization mode) method, with limits of quantitation of 5 nG_sub>5L (plasma) and 25 nG_sub>5L (urine), respectively. BAY 38-7271 was used as an internal standard. Plasma concentrations of BAY 38-7271 increased proportionally to the dose until the end of infusion, with small to moderate inter-individual variability. Statistical analysis of Cmax and normal values supported the linear pharmacokinetic hypothesis. The maximum plasma concentrations ranged from 75.7 nG5L (5 μg) to 1870 nG5L (120 μg; geometric mean). The decline in drug concentration after infusion could be described by a three-compartment model, with distribution half-lives (t1) of 0.21 and 1.81 hours (major half-life), respectively. In the highest dose groups (40–120 μg), the terminal half-life was 8–12 hours. The volume of distribution (V_ss) of BAY 38-7271 is relatively large, ranging from 1.72 to 2.79 μL/kg, consistent with animal experimental data (see Table 2). Unmetabolized BAY 38-7271 was not detected in urine. After continuous infusion to steady state, the expected plasma concentration (CP,ss) of BAY 38-7271 ranged from 150 nGu/L (5 μGu/h) to 3600 nGu/L (120 μGu/h) (calculated by dividing the infusion rate by the clearance rate of 33.3 μL/h). [1] BAY 38-7271 is a highly potent and selective CB1/CB2 receptor agonist that has shown significant neuroprotective effects in various models. Administering BAY 38-7271 via 4-hour or 15-minute infusions 5 hours after injury also showed neuroprotective effects. The dose of BAY 38-7271 required to achieve maximum neuroprotective effect is significantly lower than the dose that can induce typical cannabinoid-like side effects. Therefore, this compound is expected to provide a novel treatment with a good therapeutic window for traumatic brain injury (TBI) and cerebral ischemia. Preliminary studies in healthy male subjects showed that BAY 38-7271 is safe and well-tolerated. [1]

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- Mechanism of action: BAY 38-7271 activates CB1 receptors, inhibits the adenylate cyclase-cAMP pathway, reduces the release of neurotransmitters such as glutamate, and modulates the activity of ion channels, thereby exerting a neuroprotective effect in TBI. [1]
- Indications: Primarily used to treat traumatic brain injury, aiming to reduce brain damage and improve neurological function after injury. [1]

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Traumatic brain injury (TBI) is the most common cause of death and disability among adults under 40 years of age in developed countries; globally, the incidence of TBI is rising, with approximately 9.5 million people hospitalized for TBI each year and an estimated death toll exceeding 1 million [1].
BAY 38-7271 promises to provide a novel treatment with a good therapeutic window for TBI or cerebral ischemia [1].

C20H21O5F3S

430.43794

430.106

C, 55.81; H, 4.92; F, 13.24; O, 18.59; S, 7.45

212188-60-8

9845561

Solid powder

1.351 g/cm3

527.206ºC at 760 mmHg

272.645ºC

5.317

1

8

8

29

619

1

FC(CCCS(OC1C=CC=C(OC2=CC=CC3CC(CC2=3)CO)C=1)(=O)=O)(F)F

XJURALZPEJKKOV-CQSZACIVSA-N

InChI=1S/C20H21F3O5S/c21-20(22,23)8-3-9-29(25,26)28-17-6-2-5-16(12-17)27-19-7-1-4-15-10-14(13-24)11-18(15)19/h1-2,4-7,12,14,24H,3,8-11,13H2/t14-/m1/s1

[3-[[(2R)-2-(hydroxymethyl)-2,3-dihydro-1H-inden-4-yl]oxy]phenyl] 4,4,4-trifluorobutane-1-sulfonate

BAY 38-7271; BAY-38-7271; 212188-60-8; BAY-38-7271; 1-Butanesulfonic acid, 4,4,4-trifluoro-, 3-(((2R)-2,3-dihydro-2-(hydroxymethyl)-1H-inden-4-yl)oxy)phenyl ester; SRX4T6TMUS; UNII-SRX4T6TMUS; BAY 38-7271; CHEMBL1668508; BAY-387271; BAY387271; (-)-Bay-38-7271; KN 387271; KN-387271; KN387271; UNII-SRX4T6TMUS

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

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.)