In cell models of adipocytes (3T3-L1), hepatocytes (HepG2), and myotubes (C2C12), imidacloprid decreases insulin-stimulated overdose. Adenosine B (AKT), one of the primary controllers of insulin signaling, was phosphorylated less when imidacloprid was administered, but overall AKT expression remained same. Ribosomal S6 (S6K), a downstream target of AKT and a feedback amplifier of insulin signaling, is phosphorylated less when imidacloprid is applied [1].

Increased imidacloprid dosages have been shown to decrease cognitive function, particularly in young animals. These effects may be attributed to altered expression of relevant genes. At both the 2 and 8 mg/kg doses, there was a significant reduction in the learning activities of the infant model group; the learning activities decreased even further at the 8 mg/kg level. Additionally, it was discovered that there had been no discernible changes to the expression levels of GRIN1, SYP, and GAP-43 [2]. In zebrafish, early developmental behavioral exposure to imidacloprid exerts an early and long-lasting impact on brain function. Imidacloprid treatment throughout the growth stage dramatically decreases novel pond exploration in adolescent larvae and increases motor-sensory responses to startle stimuli in fish [3]. At 20 mg/kg/day, there was a noticeable decrease in the amount of body weight gained, and the relative body weights measured during necropsy, implanted, and at this point also increased considerably at this level. Both spontaneous locomotor activity and hematological and body weight indicators rose at the highest dosage exposure. Imidacloprid at high doses caused degenerative alterations in the kidneys, liver, and brain [4]. Imidacloprid at a dose of 20 mg/kg significantly altered myocardial SOD, CAT, GPx, GSH, and LPO; it also significantly affected brain SOD, CAT, and GPx, as well as renin LPO [5]. At high dosages, imidacloprid inhibited cell-mediated immune responses, as seen by the decreased DTH response and decreased T pathway stimulation index of PHA. Histopathological study of mice footpad sections demonstrated dose-related suppression of DTH responses; significant histopathological alterations were also seen in the heart and spleen [6].

Absorption, Distribution and Excretion
/Milk/ A 41 kg lactating goat was administered 10 mg/kg of [(14)C-methylene]imidacloprid daily for three consecutive days via intubation. The goat was euthanized 2 hours after the last administration. The highest plasma concentration was 3.98 mg/mL 2 hours after the last administration. The highest radioactive concentrations in milk were 3.16–3.65 μg/g 8 hours after the first administration and 2 hours after the third administration; the concentration in milk before the second administration was 2.77 μg/g. Assuming a daily milk production of approximately 2 liters, the radioactivity in milk was approximately 0.4% of the total administered dose. The total residual radioactivity in edible tissues and organs was approximately 5% of the administered dose 2 hours after the third administration. The residual radioactivity in edible tissues were: liver 1.3%, kidney 0.1%, muscle 3%, and fat 0.4%. The main compounds found in milk and edible tissues were imidacloprid, olefin imidacloprid (NTN 35884), and 4- and 5-hydroxyimidacloprid. Five laying hens were administered 10 mg/kg of methylene-labeled 14C-imidacloprid via gavage for three consecutive days. The highest radioactivity concentration in plasma was observed 0.5 hours after the third administration, at 0.34 μg/mL. At this point, the total residual amount in edible tissues and organs was approximately 3% of the total dose. The highest radioactivity concentration in eggs was observed 2 hours after the last administration, at 1.347 μg/g. This concentration was less than 0.2% of the total administered dose. The main metabolite in eggs was olefin imidacloprid. Olefin and denitrified imidacloprids were detected in muscle and kidney tissues. A: NTN 33893, purity 99.9%; B: 1-[(6-chloro-3-pyridyl)(14)C-methyl]-4,5-dihydro-N-nitro-1H-imidazol-2-amine] (150.7 uCi/mg, purity >99%); Oral: Single dose (1 mg/kg B, 20 mg/kg B), multiple doses (1 mg/kg daily for 14 consecutive days, followed by a single dose of B 24 hours after the last dose); Intravenous: Single dose (1 mg/kg B); 5 doses per sex per dose In rats, 94%–100% of the administered radioactive material was absorbed after oral and intravenous administration and rapidly distributed from the central compartment to the whole body, as evidenced by its short mean absorption half-life (35 minutes) and apparent volume of distribution of approximately 84% of body volume; the short mean residence time (9–17 hours) indicates that the radioactive material is rapidly eliminated from the body; 91.4%–96% of the administered dose was excreted in urine and feces within 48 hours after oral or intravenous administration; no significant radioactive material was detected in exhaled breath; high concentrations of total radioactive material were observed in the kidneys, liver, lungs, and skin; no signs of bioaccumulation were found. [Imidazolidine-4,5-(14)C] Imidacloprid (0.827 μCi/mg, purity 99.8%, ... and 124 μCi/mg, purity >99%...); orally; 1 mg/kg (10 male rats, 5 female rats) and 150 mg/kg (5 male rats); rapid absorption after oral administration, with the low-dose group reaching maximum plasma concentrations within 1 to 1.5 hours and the high-dose group reaching maximum plasma concentrations within 4 hours; the renal excretion fraction (91%) of the administered dose was higher than that of methylene-labeled imidacloprid (75%) after oral administration of the imidazoline-labeled compound; less fecal excretion, with 1% of the administered radioactivity remaining in the body after 48 hours; the highest radioactivity concentrations were reported in the liver regardless of the dose level; 5 metabolites were identified in the urine, accounting for 77% of the radioactivity recovered in the urine. For more complete data on the absorption, distribution, and excretion of midaclopyridine (10 in total), please visit the HSDB record page. Metabolites/Metabolites A: NTN 33893, 99.9% purity; B: 1-[(6-chloro-3-pyridyl)(14)C-methyl]-4,5-dihydro-N-nitro-(1)H-imidazol-2-amine] (150.7 uCi/mg, >99% purity); Oral: Single dose (1 mg/kg B, 20 mg/kg B), multiple doses (1 mg/kg A once daily for 14 days, followed by a single dose of B 24 hours after the last dose); Intravenous: Single dose (1 mg/kg B); 5 doses per sex per dose In rats, over 90% of the radioactive material was cleared within 48 hours of administration, with less than 1% remaining in the carcass across all dose groups. No sex differences were observed in excretion patterns and excretory metabolic profiles after low-dose administration; however, at high doses, renal clearance was slightly higher in females than in males. Males metabolized the test compound more readily, with lower levels of the parent compound compared to females. Oxidative cleavage of the parent compound yielded 6-chloronicotinic acid, which reacted with glycine to form a conjugate (WAK 3583). A second major metabolic pathway involved hydroxylation and dehydration of the imidazolidine ring at the 4- or 5-position, yielding the metabolite NTN 35884. These metabolites were excreted in urine and feces. No evidence of bioaccumulation after repeated administration was reported.
Methylene-[(14)C]imidacloprid (86.4–123 uCi/mg, purity 98.4–99%): single dose [1 mg/kg (5 males), 150 mg/kg (7 males)], and long-term (1 year) administration of unlabeled imidacloprid in feed prior to radiolabeled imidacloprid (80 mg/kg, 10 males); Methylene-[(14)C]WAK 3839 (40 uCi/mg, purity 99%): 1 mg/kg (5 males); both compounds were rapidly absorbed after a single oral dose; the terminal half-lives of imidacloprid and WAK 3839 were 35.7 h and 46.9 h, respectively; 75% of the administered dose of both compounds was excreted primarily in urine within 48 hours; fecal excretion was less significant, with 21% and 16% excreted, respectively. The recovered radioactive material was excreted through this route; glycine conjugate of 6-chloronicotinic acid (WAK 3583), two monohydroxylated metabolites (WAK 4103), and an unsaturated metabolite (NTN 35884) were identified in urine, accounting for 82% of the total radioactivity; the same metabolites were also identified in feces; in addition to the unchanged WAK 3839, another metabolite, NTN 33823, was also identified in the urine and feces of rats treated with WAK 3839; WAK 3839 and other metabolites identified after a single low-dose administration were detected in the urine of rats and mice fed a diet containing imidacloprid for a long period of time; the results of this study indicate that WAK 3839 is formed during long-term exposure to imidacloprid.
WAK 3839 is a metabolite of NTN 33893; purity 98.9%; /V79-HGPRT assay, dosage (based on solubility limits and cytotoxicity assays): -S9 assay and one of two +S9 assays at doses of 500, 1000, 1500, 1750, and 2000 ug/mL, respectively; the other +S9 assay at doses of 500, 750, 1000, 1250, 1500, and 1750 ug/mL; after seeding 4 x 10⁶ cells/250 mL culture flasks, cells were exposed to the test substance (-/+S9 microsomes) for 5 hours, followed by an exponential growth phase “expression phase”, and then reseeded under selective conditions (10 μg/mL 6-thioguanine) at a density of 3 x 10⁵ cells/100 mm culture dish; 7 After 1 day, the colonies were fixed and counted; repeated exposure cultures were performed, generating 8 replicate cultures per culture dish under selected conditions; although the positive control (-S9, ethyl mesylate; +S9, DMBA) successfully induced 6-thioguanine resistance, the test substance did not induce 6-thioguanine resistance at any dose; under these conditions, the test substance was not mutagenic in the system. Metabolites of WAK 3839 and NTN 33893; purity 94.3%; /CHO-HGPRT assay, dosage (based on solubility limit and cytotoxicity assays), -S9: 62.5, 125, 250, 500, 1000, and 2000 ug/mL; +S9: 500, 750, 1000, 1250, 1500, and 2000; After seeding 4 x 10⁶ cells/250 mL culture flasks, cells were exposed to the test substance (-/+S9 microsomes) for 5 hours, followed by an exponential growth phase “expression phase”, and then re-seeded under selective conditions (10 ug/mL 6-thioguanine) at a density of 3 x 10⁵ cells/100 mm culture dish; fixed and colonies were counted after 7 days; repeated exposure cultures were performed, with each culture dish producing 8 cells/100 mm culture dish under selective conditions. Repeat culture dishes; despite success with the positive controls (-S9, ethyl methanesulfonate; +S9, DMBA), the test samples failed to induce 6-thioguanine resistance persistently at any dose; it was not mutagenic in this system under these conditions. For more complete data on the metabolites/metabolites of imidacloprid (14 in total), please visit the HSDB record page. Known human metabolites of imidacloprid include olefins, 5-hydroxyimidacloprid, and 1H-imidazol-2-amine, 1-[(6-chloro-3-pyridyl)methyl]-4,5-dihydro-N-nitroso-.

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Biological Half-Life
The excretory half-life of radiolabeled imidacloprid in rats was calculated after a single intravenous injection of 1 mg/kg, a single oral administration of 1 mg/kg and 20 mg/kg, or multiple oral administrations of 1 mg/kg. The excretion half-life varies considerably (from 26 hours to 118 hours), but this variation is independent of dose, sex, or route of administration. ...
Methylene-[(14)C]imidacloprid (86.4 - 123 uCi/mg, purity 98.4 - 99%): single administration [1 mg/kg (5 males), 150 mg/kg (7 males)], and long-term (1 year) administration of unlabeled imidacloprid in feed before receiving radiolabeled imidacloprid (80 mg/kg, 10 males); Methylene-[(14)C]WAK 3839 (40 uCi/mg, purity 99%): 1 mg/kg (5 males); both compounds were rapidly absorbed after a single oral administration; the terminal half-lives of imidacloprid and WAK 3839 were 35.7 hours and 46.9 hours, respectively...
...bees were given oral administration of imidacloprid at doses of 20 and 50 μg/kg, respectively. ...Imidacloprid has a half-life of 4.5 to 5 hours and is rapidly metabolized into 5-hydroxyimidacloprid and olefins. ...

Toxicity Summary
Identification and Uses: Imidacloprid (IM) forms colorless crystals. It is registered as an insecticide in the United States, but approved insecticide uses may change periodically, so it is essential to consult federal, state, and local authorities for currently approved uses. IM is used to control pests on crops and nursery crops, building pests, and parasites on companion animals. Human Contact and Toxicity: The most common clinical symptoms include: rash, difficulty breathing, headache, tearing, nausea, itching, dizziness, increased salivation, vomiting, numbness, and dry mouth. One case of worker poisoning due to imidacloprid splashing into the eyes has been reported. Clinical symptoms included burning eyes and corneal abrasions. In two fatal cases, IM blood concentrations were detected at 12.5 and 2.05 μg/mL, respectively. Damage to HepG2 cells by imidacloprid is caused by the insecticide's chromosome breakage effect (76.6% of cells in the micronucleus assay showed no centromere signal). Animal studies: Imidacloprid with a purity of 94.2% was non-irritating to rabbit eyes and skin, and non-sensitizing to guinea pig skin. A single oral dose of imidacloprid showed moderate toxicity in rats and mice. Oral administration of ≥200 mg/kg body weight to rats and ≥71 mg/kg body weight to mice resulted in behavioral and respiratory symptoms, motor disturbances, narrowing of the palpebral fissure, transient tremors, and spasms. These clinical symptoms resolved within 6 days. In chronic studies in rats, the liver was the primary target organ, with hepatocyte hypertrophy and sporadic cell necrosis observed only in high-dose male rats. Liver pathological changes were mild at the end of the study and were completely reversible during the recovery period. Histopathological changes were observed in the testes and epididymis of IM-treated male rats. In rat developmental studies, a higher proportion of male fetuses and an increased incidence of wavy ribs were observed. In rabbit developmental studies, decreased fertility was observed in the high-dose group based on increased abortion, litter resorption, and post-implantation loss due to increased late resorption. However, this dosage level also led to reduced body weight and weight gain, and increased mortality. Early developmental exposure to IM in zebrafish had early and lasting effects on neurobehavioral function. In vivo treatment of rats with 170 mg/kg IM and subsequent microscopic observation of bone marrow cells identified chromosomal structural aberrations, abnormal cells, and mitotic index. Male rats, in particular, showed susceptibility to the genotoxicity of imidacloprid. Ecotoxicity studies: The effects of IM on beneficial insects such as bees (Apis mellifera L.) remain controversial. At concentrations common in agricultural ecosystems, IM application reduced the sensitivity of juvenile bees to rewards and impaired their associative learning abilities. Therefore, once nectar containing traces of IM enters the hive, it may impair bee work within the hive, negatively impacting the overall performance of the colony. Neuronal apoptosis was detected using TUNEL DNA labeling when laboratory-raised adult worker bees were treated with sublethal doses of IM. This study investigated the effects of IM and 5-OH-IM on bee behavior at two different times of the year using olfactory conditioning. The results showed that the learning ability of winter honeybees treated with long-term IM and 5-OH-IM decreased. The lowest effective concentration of IM in summer honeybees (12 μg/kg) was lower than that in winter honeybees (48 μg/kg), indicating that summer honeybees were more behaviorally sensitive than winter honeybees. This study also investigated the acute and chronic oral toxicity of IM and its major metabolites (5-hydroxyimidacloprid, 4,5-dihydroxyimidacloprid, denitrified imidacloprid, 6-chloronicotinic acid, olefins, and urea derivatives) in Western honeybees (Apis mellifera). Acute poisoning by IM or its metabolites led to the rapid onset of neurotoxic symptoms, such as hyperresponsiveness, hyperactivity, and tremors, eventually resulting in lethargy and sluggishness. Compared with untreated colonies, bumblebee (Bombus terrestris audax) colonies exposed to IM showed defects in both colony growth and nest condition. In a breeding study of mallards, eggshell thickness was affected when the concentration of IM in the feed was greater than or equal to 61 mg/kg; at a concentration of 241 ppm, the weight gain of female mallards was reduced by 52%. In an early life cycle study of rainbow trout, treatment-related declines in growth and survival were observed when the treatment concentration was ≥1.2 mg ai/L.

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Toxicity Data
LC50 (Rats)> 5,323 mg/m³/4h

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Interactions
Standard ecotoxicological risk assessments are conducted on single substances; however, monitoring of streams in agricultural areas indicates that pesticides are rarely present alone. In fact, brief but intense pulse events, such as storm runoff and spray drift during application, can expose freshwater environments to high concentrations of complex pesticide mixtures. This study investigated the potential risks of non-target aquatic organisms exposed to a mixture of the neonicotinoid pesticides imidacloprid and thiamethoxam, and the pyrethroid pesticides deltamethrin and lambda-cyhalothrin, compared to single-substance exposure. All four pesticides were detected in water bodies at concentrations above baseline. These pesticides are known to have adverse effects on non-target aquatic organisms under single-substance exposure conditions. In this study, first-instar larvae of the non-target aquatic organism Chironomus riparius were exposed to a mixture of these four pesticides at concentrations of 50% of their 96-hour median lethal concentration (LC50) for one hour. The larvae were then reared to adults under uncontaminated conditions, and their survival, developmental time, and reproductive capacity were assessed. The results showed that the risk of disturbance to the survival and development of non-target aquatic organisms under this condition was not negligible, given the significantly increased mortality rates in most pesticide-exposed groups and the delayed development following pyrethroid exposure. Although the pesticide combination did not appear to exacerbate any harmful effects, there is evidence of antagonistic effects. No effects on reproductive capacity were observed with any of the pesticide treatments. Previous studies have confirmed the oxidative and neurotoxic effects of the neonicotinoid insecticide imidacloprid on various animal species. The primary objective of this study was to determine how the metabolic regulators synergist ether and menadione affect the hepatotoxicity of imidacloprid in male and female Sprague-Dawley rats. Animals were exposed alone to imidacloprid (170 mg/kg) or in combination with synergist ether (100 mg/kg) or menadione (25 mg/kg) for 12 and 24 hours. Spectrophotometric analysis was performed on the specific activities of glutathione peroxidase, glutathione S-transferase, catalase, and total cholinesterase, as well as the total glutathione content, total protein content, and lipid peroxidation levels in liver and kidney homogenates. In male rats, imidacloprid exhibited pro-oxidative and neurotoxic effects primarily in the kidneys after 24 hours of exposure. Our results suggest that the observed differences in the pro-oxidative and neurotoxic effects of imidacloprid may be related to its metabolic differences between sexes. Co-exposure with piperine or menadione (90-minute pretreatment) revealed tissue-specific effects of imidacloprid on total cholinesterase activity. The increase in cholinesterase activity in the kidneys may be an adaptive response to imidacloprid-induced oxidative stress. In the liver of male rats, co-exposure with piperine or menadione exacerbated imidacloprid toxicity. In female rats, co-exposure with imidacloprid and menadione resulted in pro-oxidative effects, while no such effects were observed with imidacloprid or menadione alone. In conclusion, the sex-, tissue-, and time-of-action specific effects of imidacloprid are a significant characteristic of its toxicity. This study used an acute toxicity test on earthworms to investigate the combined toxicity of five insecticides (chlorpyrifos, abamectin, imidacloprid, lambda-cyhalothrin, and phoxim), two herbicides (atrazine and butachlor), and one heavy metal (cadmium). The toxicological interactions of these chemicals in four-, five-, six-, seven-, and eight-component mixtures were investigated using the Combination Index (CI) equation method. In the four- and five-component mixtures, a synergistic effect predominated at low effect levels, while the interaction patterns in the six-, seven-, and eight-component mixtures exhibited synergistic effects. The combination of lambda-cyhalothrin + imidacloprid + butachlor + atrazine + chlorpyrifos + phoxim showed the strongest synergistic effect, with CI values ranging from 0.09 to 0.15. The nature of the interactions varied with effect levels, and the correlation of synergistic effects increased with increasing mixture complexity. We compared the CI method with classical concentration-additive (CA) and independent-action (IA) models, finding that the CI method can accurately predict combined toxicity. The predicted synergistic effects were caused by the co-occurrence of pesticides and heavy metals, especially at low effect levels, which may have significant implications for risk assessment in real-world terrestrial environments. Metabolic modifiers and other agents have been shown to alter the toxicity of imidacloprid. The CYP450 inhibitor piperonyl butyl ether enhanced the toxicity of imidacloprid. In subchronic and chronic feeding studies, mice developed anaphylactic reactions to ether, which is used as an anesthetic for procedures such as blood draws and tattooing. These animals developed respiratory distress, respiratory failure, and convulsions shortly after ether injection and died. The specific mechanism by which imidacloprid induces ether anaphylaxis is currently unknown.
For more complete data on imidacloprid interactions (6 items), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 for male rats: 424 mg/kg
Oral LD50 for female rats: 450-475 mg/kg
Oral LD50 for male mice: 131 mg/kg
Oral LD50 for female mice: 168 mg/kg
For more complete data on imidacloprid non-human toxicity values (18 items), please visit the HSDB record page.

[1]. Imidacloprid, a neonicotinoid insecticide, induces insulin resistance. J Toxicol Sci. 2013;38(5):655-60.

[2]. Insecticide imidacloprid influences cognitive functions and alters learning performance and related gene expression in a rat model. Int J Exp Pathol. 2015 Oct;96(5):332-7.

[3]. Neurobehavioral impairments caused by developmental imidacloprid exposure in zebrafish. Neurotoxicol Teratol. 2015 May-Jun;49:81-90.

[4]. A 90 days oral toxicity of imidacloprid in female rats: morphological, biochemical and histopathological evaluations. Food Chem Toxicol. 2010 May;48(5):1185-90.

[5]. Effect of imidacloprid on antioxidant enzymes and lipid peroxidation in female rats to derive its No Observed Effect Level (NOEL). J Toxicol Sci. 2010 Aug;35(4):577-81.

[6]. Immunotoxic effects of imidacloprid following 28 days of oral exposure in BALB/c mice. Environ Toxicol Pharmacol. 2013 May;35(3):408-18.

(E)-Imidacloprid is the E-isomer of imidacloprid. Imidacloprid is a neonicotinoid insecticide, belonging to a class of neuroactive insecticides that mimic nicotine. It is a proprietary chemical manufactured by Bayer Crop Science (a Bayer AG) and marketed under trade names such as Kohinor, Admire, Advantage, Gaucho, Merit, Confidor, Hachikusan, Premise, Prothor, and Winner. Its uses include pest control, seed treatment, insecticidal spraying, termite control, flea control, and systemic insecticide application. See also: imidacloprid; moxifloxacin (ingredient); imidacloprid; ivermectin (ingredient).

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Therapeutic Uses
Cholinergic drugs; insecticides
/Clinical Trials/ ClinicalTrials.gov is a registry and results database that tracks human clinical studies funded by public and private institutions worldwide. This website is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each record on ClinicalTrials.gov contains a summary of the study protocol, including: the disease or condition; the intervention (e.g., the medical product, behavior, or procedure being studied); 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 (for providing patient health information) and PubMed (for providing citations and abstracts of academic articles in the medical field). Imidacloprid is included in this database.
(Veterinary): Ectopicidal agent.

C9H10CLN5O2

255.66

255.052

138261-41-3

Imidacloprid-d4;1015855-75-0

86287518

White to off-white solid powder

1.6±0.1 g/cm3

442.3±55.0 °C at 760 mmHg

144ºC

221.3±31.5 °C

0.0±1.1 mmHg at 25°C

1.706

-0.43

1

4

2

17

319

0

C1CN(/C(=N/[N+](=O)[O-])/N1)CC2=CN=C(C=C2)Cl

YWTYJOPNNQFBPC-UHFFFAOYSA-N

InChI=1S/C9H10ClN5O2/c10-8-2-1-7(5-12-8)6-14-4-3-11-9(14)13-15(16)17/h1-2,5H,3-4,6H2,(H,11,13)

(NE)-N-[1-[(6-chloropyridin-3-yl)methyl]imidazolidin-2-ylidene]nitramide

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 (~391.14 mM)
H2O : ~1 mg/mL (~3.91 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (9.78 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 (9.78 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in 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 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 (9.78 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.)