Phosphatidylinositide 3-kinase (PI3K)
Protein kinase C zeta (PKCζ)
Extracellular signal-regulated kinase (ERK)
cAMP response element-binding protein (CREB)
Protein kinase B (Akt) [1]

After administration of Erucic acid (3 mg/kg, p.o.), the phosphorylation levels of PI3K, PKCζ, ERK, CREB, and Akt in the mouse hippocampus are significantly increased compared with the vehicle-treated control group (pPI3K: \(t=2.489\), \(P<0.05\); pPKCζ: \(t=4.441\), \(P<0.05\); pERK: \(t=3.744\), \(P<0.05\); pCREB: \(t=4.380\), \(P<0.05\); pAkt: \(t=3.669\), \(P<0.05\)) [1]
The phosphorylation level of CaMKII in the hippocampus is not affected by erucic acid [1]

In the hippocampal regions, erucic acid (oral; 3 mg/kg) increased phosphorylation levels of PI3K, PKC z, ERK, CREB, and Akt in contrast to vehicle-treated controls [1].

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In normal naïve mice, Erucic acid (3 mg/kg, p.o.) enhances memory performance in the passive avoidance task, significantly increasing the retention trial latency compared with the vehicle control group (\(F(3,33)=3.609\), \(P<0.05\)) [1]
In scopolamine-induced (1 mg/kg, i.p.) memory-impaired mice, erucic acid (3 mg/kg, p.o.) ameliorates cognitive deficits: it reverses the reduced retention latency in the passive avoidance task (\(F(5,53)=19.78\), \(P<0.05\)), increases the spontaneous alternation percentage in the Y-maze task (\(F(5,48)=5.064\), \(P<0.05\)), and does not affect total arm entries (locomotor activity) [1]
In the Morris water maze task, erucic acid (3 mg/kg, p.o.) reduces the escape latency of scopolamine-treated mice on training days 4 and 5 (day 4: \(F(3,27)=6.736\), \(P=0.0015\); day 5: \(F(3,27)=11.14\), \(P<0.0001\)); in the probe trial, it recovers the reduced swimming time in the target quadrant without affecting swimming speed (\(F(3,27)=0.8766\), \(P=0.4655\)) or total distance moved (\(F(3,27)=2.157\), \(P=0.1164\)) [1]

Hippocampal protein phosphorylation detection (Western blot): Mice are sacrificed 1 hour after erucic acid administration, and the hippocampus is isolated. The tissue is homogenized in ice-cold Tris–HCl buffer containing sucrose, EDTA, EGTA, PMSF, sodium orthovanadate, and protease inhibitor. After protein quantification, 15 μg of protein is subjected to SDS-PAGE (8% gels) under reducing conditions, then transferred to PVDF membranes. Membranes are blocked with 5% skim milk, incubated with primary antibodies (anti-pPI3K, anti-PI3K, anti-pAkt, anti-Akt, anti-pPKCζ, anti-PKCζ, anti-pERK, anti-ERK, anti-pCREB, anti-CREB) at 4 °C overnight, followed by horseradish peroxidase-conjugated secondary antibodies. Immunoreactivity is detected via enhanced chemiluminescence and analyzed with imaging software [1]

Animal/Disease Models: normal young mice [1]
Doses: 3 mg/kg
Route of Administration: po (po (oral gavage)) 3 mg/kg
Experimental Results: Enhanced phosphorylation levels of hippocampal PI3K, PKC z, ERK, CREB and Akt.

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Passive avoidance task: Male ICR CD-1® mice (25–30 g, 6 weeks old) are housed 5 per cage (27×22×14 cm) with ad libitum food and water, maintained on a 12-h light/dark cycle (23±1 °C, 60±10% humidity). For memory enhancement study: Erucic acid (1, 3, 10 mg/kg, p.o., suspended in 10% Tween 80) or vehicle is administered 1 h before acquisition trial. Mice are placed in the light chamber, and 10 s later the guillotine door is opened; when entering the dark chamber, a 0.25 mA foot shock is applied for 3 s, and acquisition latency (max 60 s) is recorded. Retention latency (max 600 s) is measured 24 h later. For memory deficit amelioration study: Erucic acid (1, 3, 10 mg/kg, p.o.) or donepezil (5 mg/kg, p.o.) is administered 1 h before acquisition trial, and scopolamine (1 mg/kg, i.p.) is given 30 min before acquisition. Acquisition latency is recorded (max 60 s, forced entry if needed), and a 0.5 mA foot shock is applied; retention latency (max 300 s) is measured 24 h later [1]
Y-maze task: Mice are administered erucic acid (1, 3, 10 mg/kg, p.o.), donepezil (5 mg/kg, p.o.), or vehicle 1 h before the trial, and scopolamine (1 mg/kg, i.p.) 30 min before. Mice are placed in one arm of the Y-maze (40×3×12 cm arms, 120° angle), and arm entries are recorded for 8 min. Spontaneous alternation percentage is calculated as (unrepeated alternations / total entries - 2) × 100. The maze is cleaned with 70% ethanol between tests [1]
Morris water maze task: Mice are subjected to 7-day tests (habituation, 5-day training, probe trial). The pool (90 cm diameter, 45 cm height) is filled with 22–24 °C water (darkened with black food coloring) to 30 cm. Habituation: Mice swim for 60 s without a platform. Training: A platform (6 cm diameter, 29 cm height) is placed in the target quadrant. Erucic acid (3 mg/kg, p.o.), donepezil (5 mg/kg, p.o.), or vehicle is administered 1 h before the first daily training (2 trials/day); scopolamine (1 mg/kg, i.p.) is given to all groups except control 30 min before training. Escape latency (max 60 s) is recorded. Probe trial: Platform is removed, and mice swim for 60 s; swimming time in target quadrant, speed, and total distance are measured [1]
Western blot animal preparation: Mice are administered erucic acid (3 mg/kg, p.o.) or vehicle, sacrificed by cervical dislocation 1 h later, and the hippocampus is isolated for protein extraction [1]

Absorption, Distribution and Excretion
Following injection of 14C-erucic acid emulsion from rapeseed oil, the highest concentration of erucic acid was observed in rat liver lipids, followed by the spleen and kidneys. Lipid uptake of fatty acids was lower in the brain, testes, and seminal vesicles. In male rats fed erucic acid for 20 consecutive days, erucic acid was incorporated into diphosphatidylglycerols and synthetic phospholipids in the heart and liver. In Wistar rats, a single oral administration of 560 mg erucic acid (ethyl ester)… peak erucic acid levels in the stomach and small intestine (40% of the dose) were reached 2 hours after administration. Peak erucic acid levels in the colon (50% of the dose) were reached 8 hours after administration. This indicates low absorption of erucic acid. Peak erucic acid levels in cardiac blood (14% of total fatty acids, compared to a background level of 2.5%) were reached 2 hours after administration. Male Wistar rats were intravenously injected with a mixture of free 14C-labeled erucic acid and 3H-labeled oleic acid. Radioactivity was measured in blood, liver, heart, kidney, and spleen at 2, 4, 8, 16, and 30 minutes. At all time points, most of the radioactivity was found in the liver, primarily in the form of triglycerides (60% of total lipid radioactivity) and phospholipids (20% to 30%). Radioactivity was 10 to 15 times lower in other organs than in the liver. In the heart, the 14C content was 3 to 4 times that of 3H. More than 80% of the radioactive material was found in triglycerides. In the spleen and kidney, the (14)C:(3)H ratio of free fatty acids and monoglycerides was particularly high. In the kidneys, 60% of (14)C exists as nervonic acid in monoglycerides and 40% in phospholipids, indicating that the mononervonic acid formed is used for phospholipid biosynthesis. For more complete data on the absorption, distribution, and excretion of erucic acids (12 in total), please visit the HSDB record page.
Metabolism/Metabolites
Rats fed rapeseed oil (containing 46.2% erucic acid) for 20 weeks showed a 2-fold increase in cardiac sphingomyelin content. Following high-erucic acid rapeseed oil feeding, 22:1 was incorporated into cardiophospholipids (5.6%) and sphingomyelin (10.5%)…
Male Wistar rats were fed erucic acid for 20 consecutive days. Erucic acid was incorporated into diphosphatidylglycerols and sphingomyelins in the heart and liver. Erucic acid levels in the heart, incorporating triglycerides and free fatty acids, were higher than in the liver.
A study using normal controls and Zellweger fibroblast cultures showed that peroxisomes play an important role in the chain shortening (β-oxidation) of erucic acid.
Male Sprague-Dawley rats were fed diets containing different levels of erucic acid (22:1 n-9) for one week. Increased dietary 22:1 n-9 content led to a significant increase in myocardial lipid deposition, which was confirmed by histological assessment and accumulation of 22:1 n-9 in cardiac lipids; no increase in cardiac triglyceride content was observed except when fed high-erucic acid rapeseed oil (42.9% 22:1 n-9).
For more complete data on the metabolism/metabolites of erucic acid (15 in total), please visit the HSDB record page.

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Eucricic acid can easily cross the blood-brain barrier (BBB) [1]

Interactions
This study aimed to evaluate the ability of propionyl-L-carnitine to prevent erucic acid-induced cardiac injury. Rats were fed a normal diet or a diet supplemented with 10% erucic acid for 10 days, with or without intraperitoneal injection of propionyl-L-carnitine (1 mM/kg/day for 10 days). Erucic acid diets led to increased levels of triglycerides (from 5.6 mg/gww to 12.4 mg/gww, P < 0.01) and free fatty acids (from 2.0 mg/gww to 5.1 mg/gww, P < 0.01), but no change in phospholipid levels. There was no difference in cardiac mechanical activity between the two groups during aerobic perfusion using isovolumetric perfusion. Conversely, when pressure-volume curves were measured, the cardiac output of rats in the erucic acid-treated group was reduced. Regardless of diet, propionyl-L-carnitine treatment consistently produced a positive inotropic effect. This was accompanied by improved mitochondrial respiration (RCI 5.1 vs 9.3, P < 0.01), increased tissue ATP content (10.3 vs 18.4 μmol/gdw, P < 0.01), and decreased triglycerides (12.4 vs 8.0 mg/gww, P < 0.01). These data suggest that long-term administration of propionyl-L-carnitine can prevent erucic acid-induced cardiotoxicity, possibly through reducing triglyceride accumulation and improving energy metabolism. Twenty-four male Wistar rats were divided into seven groups and fed daily diets containing 0, 5, 10, 15, 25, or 30 cal% rapeseed oil (relative concentrations of erucic acid were 0%, 5.5%, 11.0%, 16.5%, 22.0%, 27.5%, and 33.0% of dietary fat, respectively). All diets were supplemented with sunflower oil to bring the total to 40 calorie percentage. Eight animals from each group were sacrificed on day 3, day 6, and week 32. Microscopic examination was performed on the skeletal muscle, heart, diaphragm, and adrenal glands of each animal. Additionally, microscopic examination was performed on the thyroid gland, testes, pancreas, spleen, liver, and kidneys of animals sacrificed after 32 weeks. Growth: No significant relationship was observed between weight gain and erucic acid treatment. Animals fed 30% (calories) rapeseed oil consistently had the lowest mean weight; analysis of variance showed this difference to be nearly statistically significant by the end of the experiment. However, animals fed 20% and 25% (calories) rapeseed oil consistently had the highest mean weight. No significant relationship was observed between weight and rapeseed oil treatment. Organ weight: Some significant differences were observed between the control group and animals fed at least 15% (calories) rapeseed oil. However, no significant differences were observed related to treatment. Pathology: In animals sacrificed after 3 or 6 days, all animals fed rapeseed oil exhibited fatty degeneration of the heart, skeletal muscle, diaphragm, and adrenal glands. The severity of fatty degeneration increased with increasing rapeseed oil levels. No other abnormalities were observed. In animals sacrificed after 32 weeks, no treatment-related effects were observed in skeletal muscle, thyroid gland, pancreas, or liver in any group. Effects were observed in the kidneys—mild tubular dilation and increased intraluminal debris. These effects were most pronounced in the highest dose group. Adrenocortical cells were enlarged in doses of 10 calories and above, with the degree of enlargement increasing with increasing dose. Changes were also observed in the heart, including mild lipid deposition, myolysis foci (showing mononuclear cell proliferation), thickening of the reticular myofibril sheath, increased interstitial connective tissue components, and Anitskow cell aggregation. The severity of these effects increased with increasing rapeseed oil dose (especially in doses above 10 calories). These changes were also observed to a very mild degree in two control animals. Weaned female Sprague-Dawley rats were fed daily diets containing 0.5%, 5%, 10%, or less than 20% fat/oil: coconut oil, butter, tallow, lard, olive oil, rapeseed oil, cottonseed oil, corn oil, soybean oil, sunflower oil… At 50 days of age, the rats were given a single oral dose of dimethylbenzo[a]anthracene (DMBA). The diets were fed for 4 months… Except for the tallow group (80%) and the rapeseed oil group (77%), the tumor incidence rate in all groups (20% dose) exceeded 85%… Animals fed unsaturated fats tended to have a higher tumor incidence rate… Most tumors were adenocarcinomas. Rapeseed oil… Eight groups (5 male Wistar rats per group) were fed a diet containing 15% lipids for 12 consecutive days (free access). The treatment groups were as follows: BR+: high rapeseed acid (28% of lipids), low calcium (0.4%); BR-: low rapeseed acid (1.2% of lipids), low calcium; BR+Ca: high rapeseed acid, high calcium (9.2%); BR-Ca: low rapeseed acid, high calcium; ER+: high erucic acid (28% of lipids), low calcium; ER-: low erucic acid (1.4% of lipids), low calcium; ER+Ca: high erucic acid, high calcium; ER-Ca: high erucic acid, high calcium. The remaining lipids in each group were supplemented with corn oil. There were no significant differences among the groups in terms of individual food intake or weight gain. However, after adjusting for food intake, the results showed that the rapeseed acid group in the low calcium group had less weight gain. Weight gain in the erucic acid group was unaffected. Cardiac triglyceride and C22:1 levels were similar in all four erucic acid groups. Compared with control rats, these rats all showed mild lipid deposition in their hearts... For the brassic acid group, low calcium reduced cardiac triglyceride levels. In addition, in both high brassic acid groups, triglyceride and C22:1 cardiac levels were higher.
For more (complete) data on interactions of erucic acid (6 in total), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 in rats >19431.7 mg/kg (based on relative density of linoleic acid 0.0938).
Zebrafish LC50 710 mg/L/96 hours; conditions: semi-static.

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When used alone, erucic acid did not have a negative effect on rat survival or cardiac contractility [1]

[1]. The memory-enhancing effect of erucic acid on scopolamine-induced cognitive impairment in mice. Pharmacol Biochem Behav. 2016 Mar;142:85-90.

Erucic acid is a docosahexaenoic acid with a cis double bond at the C-13 position. It is primarily found in cruciferous vegetables—a major component of mustard oil and rapeseed oil; it is also found in broccoli, Brussels sprouts, kale, and violets. It is the conjugate acid of erucic acid. Erucic acid has been reported in white mustard (Sinapis alba), borage (Borago officinalis), and other organisms with relevant data. Erucic acid is a monounsaturated, very long-chain fatty acid with a 22-carbon backbone, its single/double bond located at the 9th position of the methyl terminus, and in a cis configuration. See also: cod liver oil (partial composition). Mechanism of Action: Mitochondrial metabolites of erucic acid inhibit the mitochondrial oxidation of other fatty acids, particularly in the heart. This may explain the accumulation of triglycerides in the hearts of rats fed rapeseed oil containing erucic acid.
The effects of erucic acid on mitochondrial oxygen uptake in the heart and liver of young rats were investigated by providing erucic acid carnitine esters (compared to palmitoyl carnitine). The presence of erucic acid carnitine significantly inhibited mitochondrial oxidation of palmitoyl carnitine. These findings suggest that mitochondrial metabolites of erucic acid inhibit the mitochondrial oxidation of other fatty acids, particularly in the heart, leading to triglyceride accumulation in the hearts of rats fed rapeseed oil. /Eucic Acid Carnitine/
The effects of high-erucic acid rapeseed oil (HER) and low-erucic acid rapeseed oil (LER) on fatty acid oxidation in rat liver were investigated. The results showed that feeding rats with erucic acid (HER) led to a decrease in hepatic palmitate oxidation capacity, and liver weight was positively correlated with dietary erucic acid content and the duration of erucic acid feeding. The inhibitory effect of erucic acid on long-chain fatty acid oxidation may be due to erucic acid incorporation into the mitochondrial membrane, interfering with the acyl-CoA transfer system on the membrane, rather than due to direct inhibition of the mitochondrial β-oxidase system.

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Therapeutic Use
/Experimental Treatment/ Ten Japanese boys with childhood adrenoleukodystrophy (ALD), one adult patient with adrenocortical neuropathy (AMN), and two asymptomatic boys with ALD received dietary erucic acid (C22:1) treatment for more than 12 months. Except for one child with ALD who died seven months after starting erucic acid treatment, serum very long chain fatty acid (VLCFA) (C24:0/C22:0) levels decreased within 1–2 months during erucic acid treatment in the remaining patients, with four patients achieving normal VLCFA levels. Neurological examination and MRI results in all 10 children with ALD showed disease progression during dietary treatment. However, the mean time from the onset of gait abnormalities to entering a vegetative state was significantly longer in the dietary treatment group than in the untreated group. One patient with adrenoleukodystrophy (AMN) showed slight improvement in spastic gait and reduced pain from lower limb spasticity. Two asymptomatic boys with ALD maintained clinical and MRI findings for 38 and 23 months, respectively, after starting dietary therapy. /Experimental Treatment/ A 5-year-old boy with rapidly progressing clinical symptoms of visual, mental, and motor impairments received lorenzo oil consisting of 1 part triglyceride and 4 parts triglyceride. After 5 months of treatment, swallowing ability improved, and T2-weighted MRI of the brain showed regression of high-signal areas in the parietal-occipital white matter. /Lorenzo Oil/
/Experimental Therapy/ A two-year open-label trial investigated the effects of oleic acid and erucic acid (Lorenzo oil) on adrenocortical neuropathy. Participants included 14 men with adrenocortical neuropathy, 5 symptomatic heterozygous females, and 5 boys with preclinical adrenocortical neuropathy. The study found no clinically meaningful benefit of the dietary therapy for patients with adrenocortical neuropathy (accumulation of very long-chain fatty acids). /Lorenzo Oil/

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Drug Warning
Researchers performed lipid analysis on brain, liver, and adipose tissue from autopsy tissues of four patients with adrenoleukodystrophy who had received a mixture of triglyceride and trierucic acid oil (“Lorenzo oil”) and compared them with seven untreated patients with adrenoleukodystrophy and three healthy controls. The dietary therapy appeared to reduce levels of saturated very long-chain fatty acids in plasma, adipose tissue, and liver; however, only one of the four patients showed a reduction in saturated very long-chain fatty acid levels in brain tissue. Although significant amounts of erucic acid remained in some tissues 12 months after discontinuation of medication, erucic acid levels in brain tissue did not exceed those in the control group at any time point. The failure of erucic acid to enter the brain in large quantities may be one reason for the poor efficacy of dietary therapy in treating adrenoleukodystrophy. /Lorenzo Oil/
Forty men and six women with adrenoleukodystrophy received treatment with lorenzo oil (20% erucic acid and 80% oleic acid). Nineteen of these patients experienced a significant decrease in platelet count. The platelet counts of the six patients with thrombocytopenia returned to normal within 2 to 3 months after discontinuation of erucic acid intake. Observations suggest that dietary management strategies for adrenoleukodystrophy requiring large amounts of erucic acid supplementation may be associated with thrombocytopenia, and that the erucic acid component in lorenzo oil may be a contributing factor to thrombocytopenia. Patients receiving erucic acid treatment should have their platelet counts closely monitored. /Lorenzo oil: 20% erucic acid and 80% oleic acid/
…This article reports the biochemical and clinical outcomes of 20 patients with X-linked adrenoleukodystrophy (ALD) during a diet based on erucic acid (C22:1). Six patients had very severe disease, nine had mild neurological symptoms, and five were asymptomatic. The baseline mean plasma C26:0 level in ALD patients was 1.41 ± 0.48 μg/mL (control group: 0.33 ± 0.12 μg/mL). C26:0 levels decreased to near normal in all patients. Despite a good response to biochemical indicators and no persistent treatment side effects, no encouraging data were observed during clinical follow-up. Asymptomatic patients remained asymptomatic for over one year after treatment. However, symptomatic patients experienced disease progression or no improvement. Fifteen men with adrenoleukodystrophy and three symptomatic heterozygous women received treatment with oleic acid and erucic acid (lorenzo oil). Five patients developed asymptomatic thrombocytopenia (platelet counts between 37,000 and 84,000/mm³), but recovered within 2 to 3 weeks after discontinuation of erucic acid. In addition, these five patients developed lymphopenia after long-term (24 to 43 months) treatment with lorenzo oil. These results suggest that long-term use of lorenzo oil to treat adrenoleukodystrophy can induce severe lymphopenia, accompanied by immunosuppression and recurrent infections. Erucic acid (cis-13-docosahexaenoic acid) is a monounsaturated ω-9 fatty acid isolated from radish (Raphanus sativus L.) seeds. [1]
It can restore the accumulation of very long chain fatty acids in the brains of patients with X-linked adrenoleukodystrophy (a neurodegenerative disease associated with dementia) to normal. [1]
Its memory-enhancing and anti-cognitive impairment effects are partly achieved by activating the PI3K-PKCζ-ERK-CREB signaling pathway and increasing the level of phosphorylated Akt in the hippocampus. [1]
In passive avoidance and Y maze tasks, its dose-response curves are inverted U-shaped, with 3 mg/kg being the optimal dose and 10 mg/kg showing poorer effects. [1]
It may be a potential drug for treating cognitive impairment-related diseases, such as…Alzheimer's disease[1]

C22H42O2

338.5677

338.318

112-86-7

63541-50-4

5281116

White to off-white <28°C powder,>32°C liquid

0.9±0.1 g/cm3

386.1±0.0 °C at 760 mmHg

28-32 °C(lit.)

349.9±15.2 °C

0.0±1.8 mmHg at 25°C

1.468

9.82

1

2

19

24

284

0

O([H])C(C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])/C(/[H])=C(/[H])\C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[H])=O

DPUOLQHDNGRHBS-KTKRTIGZSA-N

InChI=1S/C22H42O2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-20-21-22(23)24/h9-10H,2-8,11-21H2,1H3,(H,23,24)/b10-9-

(Z)-docos-13-enoic acid

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)

DMSO : ≥ 100 mg/mL (~295.36 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (7.38 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: 2.5 mg/mL (7.38 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (7.38 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)