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/ [(14)C-methylene]Imidacloprid was administered to one 41 kg lactating goat by intubation in three consecutive daily doses of 10 mg/kg. The goat was sacrificed 2 hr after the last dose. The highest plasma concentration of 3.98 mg/mL was measured after 2 hr of last dosing. The highest radioactivity of 3.16-3.65 ug/g in the milk was determined 8 hr after the first dose and 2 hours after the third dose; the concentration in the milk prior to second dosing was 2.77 ug/g. Assuming a daily milk production of about 2 liters, the radioactivity in the milk was about 0.4% of the total administered radioactivity. The total residue in the edible tissues and organs measured two hours after the third dose was about 5% of the administered radioactivity. The respective residual radioactivity in the edible tissues was 1.3% (liver), (0.1%) kidney, (3%) muscles and 0.4% (fat). The main compounds in the milk and the edible tissues were imidacloprid, olefinic imidacloprid (NTN 35884) and 4- and 5-OH-imidacloprid.
Five laying hens were intubated with 10 mg/kg methylene-labeled- (14)C-imidacloprid for 3 days. The highest radioactivity of 0.34 ug/mL in the plasma was measured at 0.5 hr after the third dosing. At that time, the total residue in the edible tissues and organs was about 3% of the total dose. The highest radioactivity of 1.347 ug/g in eggs was found 2 hr after the last dose. This level was less than 0.2% of the total administered radioactivity. The main metabolite in the eggs was the olefine-imidacloprid. Olefine- and desnitro-imidacloprid were detected in muscle and kidney tissues.
A: NTN 33893, 99.9% purity), B: 1-[(6-chloro-3-pyridinyl) (14)C-methyl]-4,5dihydro- N-nitro-1H-imidazol-2-amine] (150.7 uCi/mg, >99% purity); oral: single (1 mg/kg B, 20 mg/kg B), multiple (1 mg/kg daily for 14 days followed by 24 hr after final dose by a single dose of B); IV: single (1 mg/kg B); 5 rats/sex/dose; following oral and intravenous administration 94 - 100% of the administered radioactivity is absorbed and readily distributed to the body from the central compartment as indicated by a short mean absorption half-life (35 minutes) and an apparent volume of distribution accounting for about 84% of the total body volume; the small mean residence time which vary between 9 and 17 hours suggests that the total radioactivity is rapidly eliminated from the body; after oral or intravenous administration, 91.4 to 96% of the given dose was excreted via urine and feces by 48 hours; no significant amount of radioactivity was found in expired air; high concentrations of total radioactivity were observed in the kidney, liver, lung and skin; no signs of bioaccumulation were evident.
[Imidazolidine-4,5-(14)C] Imidacloprid (0.827 uCi/mg, 99.8% purity, ... and 124 uCi/mg, >99% purity ... ); oral; 1 mg/kg (10 male /rats/, 5 female /rats/) and 150 mg/kg (5 male /rats/); absorption after oral dosing is rapid and maximal plasma concentration is achieved between 1 and 1.5 hr at the low dose and 4 hr at the high dose; after oral administration of the imidazolidine labeled compound, the renal-excreted portion of the given dose is higher (91%) as compared to methylene labeled Imidacloprid (75%); fecal elimination plays a minor role and 1% of the administered radioactivity remains in the body at 48 hr; highest radioactivity concentrations were reported in liver irrespective of dose level; 5 metabolites were identified in urine which represent 77% of radioactivity recovered in urine.
For more Absorption, Distribution and Excretion (Complete) data for IMIDACLOPRID (10 total), please visit the HSDB record page.

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Metabolism / Metabolites
A: NTN 33893, 99.9% purity), B: 1-[(6-chloro-3pyridinyl)(14)C-methyl]-4,5-dihydro-N-nitro-(1)H-imidazol-2-amine] (150.7 uCi/mg, >99% purity); oral: single (1 mg/kg B, 20 mg/kg B), multiple (1 mg/kg A qd @ 14 days followed by 24 hrs after final dose by a single dose of B); IV: single (1 mg/kg B); 5 rats/sex/dose; >90% of administered radioactivity eliminated 48 hours after dosing with less than 1% remaining in the carcass in all dose groups; no sex differences in excretion pattern and metabolic profiles of the excreta were evident following low dose administration; however, at the high dose, females showed a slightly higher renal elimination rate than males; males showed a higher capacity to metabolize the test compound and the amount of parent compound was lower as compared to females; oxidation cleavage of the parent compound yields 6-chloronicotinic acid which then reacts with glycine to form a conjugate (WAK 3583); second major route of metabolism involves hydroxylation and elimination of water from the imidazolidine ring in the 4- or 5-position to produce the metabolite NTN 35884; these metabolites are excreted in urine and feces; no evidence of bioaccumulation following multiple dosing was reported.
methylene-[(14)C] imidacloprid (86.4 - 123 uCi/mg, 98.4 - 99% purity): single [1 mg/kg (5 males), 150 mg/kg (7 males)] and chronic treatment with the unlabeled imidacloprid for 1 year in diet prior to receiving radiolabeled imidacloprid (80 mg/kg, 10 males); methylene-[(14)C] WAK 3839 (40 uCi/mg, 99% purity): 1 mg/kg 5 males); both compound absorbed rapidly after single oral dosing; terminal half-lives for imidacloprid and WAK 3839 are 35.7 and 46.9 hrs, respectively; 75% of the given dose of both compounds are eliminated primarily via urine within 48 hrs; fecal elimination plays a minor role, since 21% and 16% of the recovered radioactivity are excreted by this route, respectively; glycine conjugate of 6-Cl-nicotinic acid (WAK 3583), two monohydroxylated metabolites (WAK 4103) and the unsaturated metabolite (NTN 35884) were identified in the urine and accounted for 82% of the total radioactivity; same metabolites were also identified in feces; besides unchanged WAK 3839, one other metabolite NTN 33823 was identified in urine and feces obtained from rats treated with WAK 3839; WAK 3839 and other metabolites identified after a single low dose were detected in urine from rats and mice treated chronically with imidacloprid in their diet; this finding suggests that WAK 3839 is formed during chronic exposure to imidacloprid.
WAK 3839, a metabolite of NTN 33893; 98.9% purity; /V79-HGPRT assay with/ doses (based on solubility limit and cytotoxicity test): 500, 1000, 1500, 1750, & 2000 ug/mL for both -S9 trials and 1 of 2 +S9 trials; for the other +S9 trial the doses were 500, 750, 1000, 1250, 1500, & 1750 ug/mL; after plating 4 x 106 cells/250 mL flask, the cells were exposed to test article (-/+ S9 microsomes) for 5 hr followed by an "expression period" of exponential growth and subsequent replating under selective conditions (10 ug/mL 6thioguanine) at 3 x 105 cells/100 mm dish; after 7 days the colonies were fixed and counted; duplicate exposure dishes were run, each dish generating 8 replicate dishes in the selection condition; test article did not induce 6-thioguanine resistance at any dose despite success of positive controls (-S9, ethyl methane sulfonate; +S9, DMBA); it is not mutagenic in this system under these conditions.
WAK 3839, a metabolite of NTN 33893; 94.3% purity; /CHO-HGPRT assay with/ doses (based on solubility limit and cytotoxicity test), -S9: 62.5, 125, 250, 500, 1000, & 2000 ug/mL; +S9: 500, 750, 1000, 1250, 1500, & 2000; after plating 4 x 106 cells/250 mL flask, the cells were exposed to test article (-/+ S9 microsomes) for 5 hr followed by an "expression period" of exponential growth and subsequent replating under selective conditions (10 ug/mL 6-thioguanine) at 3 x 105 cells/100 mm dish; after 7 days the colonies were fixed and counted; duplicate exposure dishes were run, each dish generating 8 replicate dishes in the selection condition; test article did not consistently induce 6-thioguanine resistance at any dose despite success of positive controls (-S9, ethyl methane sulfonate; +S9, DMBA); it is not mutagenic in this system under these conditions.
For more Metabolism/Metabolites (Complete) data for IMIDACLOPRID (14 total), please visit the HSDB record page.
Imidacloprid has known human metabolites that include olefin, 5-hydroxy-imidacloprid, and 1H-Imidazol-2-amine, 1-[(6-chloro-3-pyridinyl)methyl]-4,5-dihydro-N-nitroso-.

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Biological Half-Life
The half-lives for excretion of the radiolabeled imidacloprid were calculated in rats after a single i.v. dose of 1 mg/kg, after single oral doses of 1 and 20 mg/kg or after multiple doses of 1 mg/kg. The excretion half-life values varied greatly (from 26 hr to 118 hr), but the variation was not dose-, sex-, or route-dependent. ...
methylene-[(14)C] imidacloprid (86.4 - 123 uCi/mg, 98.4 - 99% purity): single [1 mg/kg (5 males), 150 mg/kg (7 males)] and chronic treatment with the unlabeled imidacloprid for 1 year in diet prior to receiving radiolabeled imidacloprid (80 mg/kg, 10 males); methylene-[(14)C] WAK 3839 (40 uCi/mg, 99% purity): 1 mg/kg 5 males); both compound absorbed rapidly after single oral dosing; terminal half-lives for imidacloprid and WAK 3839 are 35.7 and 46.9 hrs, respectively ... .
... Honeybees were treated orally with imidacloprid at 20 and 50 ug/kg per bee. ... Imidacloprid had a half-life ranging between 4.5 and 5 hr and was rapidly metabolized into 5-hydroxyimidacloprid and olefin. ...

Toxicity Summary
IDENTIFICATION AND USE: Imidacloprid (IM) forms colorless crystals. It is registered for pesticide use in the USA but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses. IM is used to control insect pests on agricultural and nursery crops, structural pests and parasites on companion animals. HUMAN EXPOSURE AND TOXICITY: The most common clinical signs included: rash, breathing difficulty, headache, tearing eyes, nausea, itching, dizziness, increased salivation, vomiting, numbness and dry mouth. One case was reported for a worker who had imidacloprid splashed into the eyes. The clinical signs were burning and corneal abrasion in the eye. IM blood concentrations found in two fatal cases were 12.5 and 2.05 ug/mL. The damage induced by imidacloprid in the HepG2 cells resulted from a clastogenic action of this insecticide (76.6% of the MN /micronucleus test/ did not present a centromeric signal). ANIMAL STUDIES: IM (purity, 94.2%) did not irritate the eyes or skin of rabbits and did not sensitize the skin of guinea-pigs. IM given orally as a single dose was moderately toxic to rats and mice. Behavioral and respiratory signs, disturbances of motility, narrowed palpebral fissures, transient trembling and spasms were seen in rats and mice treated orally at doses /greater than or equal/ to 200 mg/kg bw and /greater than or equal to/ 71 mg/kg bw, respectively. The clinical signs were reversed within 6 days. In chronic experiments conducted in rats, the liver was the principal target organ, with hypertrophy of hepatocytes and sporadic cell necrosis in high-dose males only. Liver pathology was mild at termination of the study and was fully reversible within the recovery period. IM-treated male rats showed histopathological alterations in testis and epididymis. In developmental studies in rats, there was a high percentage of male fetuses and an increased incidence of wavy ribs was observed. In a developmental rabbit study, fecundity was decreased at the high dose based on observed abortions, total litter resorptions, and increased post-implantation loss due to increased late resorptions. However, this dose level also resulted in decreases in body weight and body weight gain and produced an increase in mortality. Early developmental exposure to IM has both early-life and persisting effects on neurobehavioral function in zebrafish. Rats teated in vivo with 170 mg/kg IM, structural chromosome aberrations, abnormal cells and mitotic index were determined microscopically in bone marrow cells. Male rats in particular showed susceptibility to the genotoxic effects of imidacloprid. ECOTOXICITY STUDIES: IM effect on beneficial insects such as the honeybee Apis mellifera L is still controversial. IM administered at levels found in agroecosystems can reduce sensitivity to reward and impair associative learning in young honeybees. Therefore, once a nectar inflow with IM traces is distributed within the hive, it could impair in-door duties with negative consequences on colony performance. When laboratory-reared adult worker honey bees were treated with sublethal doses of IM, neuronal apoptosis was detected using the TUNEL technique for DNA labeling. Behavioral effects of IM and 5-OH-IM were studied using the olfactory conditioning of proboscis extension response at two periods of the year. Winter bees surviving chronic treatment with IM and 5-OH-IM had reduced learning performances. The lowest observed effect concentrations of IM was lower in summer bees (12 ug/kg) than in winter bees (48 ug/kg), which points to a greater sensitivity of honeybees behavior in summer bees, compared to winter bees. Oral acute and chronic toxicity of IM and its main metabolites (5-hydroxyimidacloprid, 4,5-dihydroxyimidacloprid, desnitroimidacloprid, 6-chloronicotinic acid, olefin, and urea derivative) were investigated in Apis mellifera. Acute intoxication by IM or its metabolites resulted in the rapid appearance of neurotoxicity symptoms, such as hyperresponsiveness, hyperactivity, and trembling and led to hyporesponsiveness and hypoactivity. Bumblebees (Bombus terrestris audax) colonies exposed to IM show deficits in colony growth and nest condition compared with untreated colonies. In mallard duck reproductive studies, effects on eggshell thickness were observed at concentrations of greater than or equal to 61 mg/kg-diet; a 52% decrease in female body weight gain was reported at 241 ppm. In the fish early-life cycle study with rainbow trout, treatment-related decreases in growth and survival were noted at concentrations of greater than or equal to 1.2 mg a.i./L.

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

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Interactions
Standard ecotoxicological risk assessments are conducted on individual substances, however monitoring of streams in agricultural areas has shown that pesticides are rarely present alone. In fact, brief but intense pulse events such as storm water runoff and spray drift during application subject freshwater environments to complex mixtures of pesticides at high concentrations. This study investigates the potential risks to non-target aquatic organisms exposed to a brief but intense mixture of the neonicotinoid pesticides imidacloprid and thiacloprid and the pyrethroid pesticides deltamethrin and esfenvalerate, compared to single substance exposure. All four of these pesticides have been detected in surface waters at concentrations higher than benchmark values and both classes of pesticides are known to exert adverse effects on non-target aquatic organisms under single substance exposure scenarios. First instar midge larvae of the non-target aquatic organism, Chironomus riparius, were exposed to combinations of these four pesticides at 50% of their LC50 (96 hr) values in a 1 hr pulse. They were then reared to adulthood in uncontaminated conditions and assessed for survival, development time and fecundity. Our results show that the risk of disruption to survival and development of non-target aquatic organisms under this scenario is not negligible on account of the significant increases in mortality of C. riparius found in the majority of the pesticide exposures and the delays in development after pyrethroid exposure. While none of the deleterious effects appear to be amplified by combination of the pesticides, there is some evidence for antagonism. No effects on fecundity by any of the pesticide treatments were observed.
Earlier research has evidenced the oxidative and neurotoxic potential of imidacloprid, a neonicotinoid insecticide, in different animal species. The primary aim of this study was to determine how metabolic modulators piperonyl butoxide and menadione affect imidacloprid's adverse action in the liver and kidney of Sprague-Dawley rats of both sexes. The animals were exposed to imidacloprid alone (170 mg/kg) or in combination with piperonyl butoxide (100 mg/kg) or menadione (25 mg/kg) for 12 and 24 hr. Their liver and kidney homogenates were analyzed spectrophotometrically for glutathione peroxidase, glutathione S-transferase, catalase, total cholinesterase specific activities, total glutathione, total protein content, and lipid peroxidation levels. Imidacloprid displayed its prooxidative and neurotoxic effects predominantly in the kidney of male rats after 24 hr of exposure. Our findings suggest that the observed differences in prooxidative and neurotoxic potential of imidacloprid could be related to differences in its metabolism between the sexes. Co-exposure (90-min pre-treatment) with piperonyl butoxide or menadione revealed tissue-specific effect of imidacloprid on total cholinesterase activity. Increased cholinesterase activity in the kidney could be an adaptive response to imidacloprid-induced oxidative stress. In the male rat liver, co-exposure with piperonyl butoxide or menadione exacerbated imidacloprid toxicity. In female rats, imidacloprid+menadione co-exposure caused prooxidative effects, while no such effects were observed with imidacloprid alone or menadione alone. In conclusion, sex-, tissue-, and duration-specific effects of imidacloprid are remarkable points in its toxicity.
The combined toxicity of five insecticides (chlorpyrifos, avermectin, imidacloprid, lambda-cyhalothrin, and phoxim), two herbicides (atrazine and butachlor) and a heavy metal (cadmium) has been examined with the earthworm acute toxicity test. Toxicological interactions of these chemicals in four, five, six, seven, and eight-component mixtures were studied using the combination-index (CI) equation method. In four-component and five-component mixtures, the synergistic effects predominated at lower effect levels, while the patterns of interactions found in six, seven, and eight-component mixtures displayed synergism. The lambda-CY+IMI+BUT+ATR+CPF+PHO combination displayed the most strongly synergistic interaction, with CI values ranging from 0.09 to 0.15. The nature of the interaction changes with the effect level and the relevance of synergistic effects increase with the complexity of the mixture. The CI method was compared with the classical models of concentration addition (CA) and independent action (IA) and we found that the CI method could accurately predict the combined toxicity. The predicted synergism resulted from co-existence of the pesticides and the heavy metal especially at low effect levels may have important implications in risk assessment for the real terrestrial environment.
Metabolic modifiers and other pharmaceutical drugs have been shown to modify the toxicity of imidacloprid. The CYP450-inhibiting piperonyl butoxide synergized the toxicity of imidacloprid. In subchronic and chronic feeding studies, mice developed hypersensitivity to ether, which was used as anesthesia during procedures such as blood withdrawal and tattooing. These animals exhibited dyspnea, respiratory failure and spasms and died shortly after administration of ether. The specific mechanism of the imidacloprid-induced hypersensitivity to ether is presently unknown.
For more Interactions (Complete) data for IMIDACLOPRID (6 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LD50 Rat (male) oral 424 mg/kg
LD50 Rat (female) oral 450-475 mg/kg
LD50 Mouse (male) oral 131 mg/kg
LD50 Mouse (female) oral 168 mg/kg
For more Non-Human Toxicity Values (Complete) data for IMIDACLOPRID (18 total), 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, which is a class of neuro-active insecticides modeled after nicotine. Imidacloprid is a patented chemical, Imidacloprid is manufactured by Bayer Cropscience (part of Bayer AG) and sold under trade names Kohinor, Admire, Advantage, Gaucho, Merit, Confidor, Hachikusan, Premise, Prothor, and Winner. It is marketed as pest control, seed treatment, an insecticide spray, termite control, flea control, and a systemic insecticide.
See also: Imidacloprid; Moxidectin (component of); Imidacloprid; Ivermectin (component of).

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Therapeutic Uses
Cholinergic Agents; Insecticides
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Imidacloprid is included in the database.
(VET): Ectoparasiticide.

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.)