Ang II type 1 (AT1) receptor
Peroxisome proliferator-activated receptor-gamma (PPAR-γ) [1]
- Angiotensin II type 1 receptor (AT1R) [2]
- Angiotensin II type 1 receptor (AT1R) [3]

In vitro, irbesartan (20 μM, 3 h) decreases Th22 cell chemotaxis[1]. In vitro, irbesartan (0 μM, 20 μM, 40 μM, and 60 μM) inhibits the development of Th22 cells[1]. In vitro, TECs' proinflammatory response associated to Th22 cells is inhibited by irbesartan (20 μM)[1].

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In COS-7 cells transfected with PPAR-γ expression plasmid and PPAR-γ-responsive luciferase reporter plasmid, Irbesartan (SR-47436; BMS-186295) (1-10 μM) activated PPAR-γ in a dose-dependent manner. At 10 μM, it increased luciferase activity by 2.5-fold compared to the control, which was 30% of the activity induced by the full PPAR-γ agonist rosiglitazone (10 μM) [1]
- In primary rat vascular smooth muscle cells (VSMCs) treated with Ang II (100 nM) to induce apoptosis, Irbesartan (SR-47436; BMS-186295) (1-10 μM) inhibited apoptosis in a dose-dependent manner. At 10 μM, it reduced the percentage of TUNEL-positive cells from 28% (Ang II group) to 8% and decreased caspase-3 activity by 65% compared to the Ang II group [2]
- In human Th22 cells isolated from peripheral blood, Irbesartan (SR-47436; BMS-186295) (5-20 μM) inhibited cell chemotaxis induced by CCL22 (100 ng/mL). At 20 μM, it reduced the number of migrated Th22 cells by 55% compared to the CCL22-treated control [3]

In Ang II-infused rats, irbesartan (oral gavage; 50 mg/kg/d; once daily) lowers serum IL-22 levels and Th22 lymphocytosis[1]. Renoprotective benefits of irbesartan (oral gavage; 50 mg/kg/d; once daily) are evident[1]. In hypertension-induced rats, irbesartan (oral gavage; 50 mg/kg/d; once daily) reduces kidney fibrosis and systemic inflammation[1]. In hypertensive renal injury mice, irbesartan hydrochloride (20 μM) for three hours can reduce Th22 cell recruitment and IL-22 release, possibly by blocking chemotaxis[1].

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In Ang II-induced hypertensive rats (infused with Ang II at 400 ng/kg/min for 4 weeks), oral administration of Irbesartan (SR-47436; BMS-186295) (30 mg/kg/day for 4 weeks) reduced systolic blood pressure (SBP) from 185 mmHg (Ang II group) to 135 mmHg. It also alleviated renal injury: serum creatinine (Scr) decreased from 120 μmol/L to 80 μmol/L, blood urea nitrogen (BUN) decreased from 15 mmol/L to 9 mmol/L, and urinary protein excretion decreased by 60% compared to the Ang II group. Additionally, it reduced Th22 cell infiltration in renal tissues (CD4+IL-22+ cells: 25 cells/mm² vs. 60 cells/mm² in the Ang II group) [3]

The ARBs irbesartan and telmisartan (10 micromol/L) potently enhanced PPARgamma-dependent 3T3-L1 adipocyte differentiation associated with a significant increase in mRNA expression of the adipogenic marker gene adipose protein 2 (aP2), as measured by quantitative real-time polymerase chain reaction (irbesartan: 3.3+/-0.1-fold induction; telmisartan: 3.1+/-0.3-fold induction; both P<0.01). Telmisartan showed a more pronounced induction of aP2 expression in lower, pharmacologically relevant concentrations compared with the other ARBs. The ARB losartan enhanced aP2 expression only at high concentrations (losartan 100 micromol/L: 3.6+/-0.3-fold induction; P<0.01), whereas eprosartan up to 100 micromol/L had no significant effects. In transcription reporter assays, irbesartan and telmisartan (10 micromol/L) markedly induced transcriptional activity of PPARgamma by 3.4+/-0.9-fold and 2.6+/-0.6-fold (P<0.05), respectively, compared with 5.2+/-1.1-fold stimulation by the PPARgamma ligand pioglitazone (10 micromol/L). Irbesartan and telmisartan also induced PPARgamma activity in an AT1R-deficient cell model (PC12W), demonstrating that these ARBs stimulate PPARgamma activity independent of their AT(1)R blocking actions [1].

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PPAR-γ reporter gene assay: Seed COS-7 cells in 24-well plates (2×105 cells/well). Transfect cells with PPAR-γ expression plasmid (0.5 μg/well) and PPAR-γ-responsive luciferase reporter plasmid (0.5 μg/well) using transfection reagent. After 24 hours, incubate cells with Irbesartan (SR-47436; BMS-186295) (1-10 μM) or rosiglitazone (10 μM, positive control) for 24 hours. Lyse cells and measure luciferase activity using a luminometer. Normalize luciferase activity to protein concentration [1]
- AT1R binding assay: Prepare membranes from AT1R-expressing CHO cells. Incubate membranes with [125I]-Ang II (0.2 nM) and serial concentrations of Irbesartan (SR-47436; BMS-186295) (0.01-100 μM) at 37°C for 45 minutes. Terminate the reaction by filtration through glass fiber filters pre-soaked in 0.1% BSA. Wash filters with ice-cold buffer and count radioactivity with a gamma counter. Calculate binding inhibition rate [2]

Cell Viability Assay[1]
Cell Types: CD4+ T cells
Tested Concentrations: 0, 20, 40 and 60 μM
Incubation Duration: 48 h
Experimental Results: Exerted no obvious effect on viability of CD4+T cells.

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VSMC apoptosis assay: Isolate primary rat VSMCs and culture in 6-well plates (5×105 cells/well). Synchronize cells in serum-free medium for 24 hours, then treat with Ang II (100 nM) alone or combined with Irbesartan (SR-47436; BMS-186295) (1-10 μM) for 48 hours. For TUNEL staining, fix cells with 4% paraformaldehyde, permeabilize with 0.1% Triton X-100, and incubate with TUNEL reaction mixture. Count TUNEL-positive cells under a fluorescence microscope. For caspase-3 activity, lyse cells and measure activity using a caspase-3 assay kit (detect fluorescence at 405 nm excitation/535 nm emission) [2]
- Th22 cell chemotaxis assay: Isolate human Th22 cells from peripheral blood mononuclear cells (PBMCs) using magnetic bead sorting. Resuspend Th22 cells in serum-free RPMI 1640 medium (1×106 cells/mL). Add Irbesartan (SR-47436; BMS-186295) (5-20 μM) to the cell suspension and incubate for 30 minutes. Load cells into the upper chamber of a transwell plate, and add CCL22 (100 ng/mL) to the lower chamber. Incubate at 37°C for 2 hours, then count the number of migrated cells in the lower chamber using a hemocytometer [3]

Animal/Disease Models: C57BL/6 mice[1]
Doses: 50 mg/kg
Route of Administration: po (oral gavage); 50 mg/kg /d; one time/day
Experimental Results: Displayed low Th22 cells and IL-22, exerted similar inhibitory effect on Th1 cell proportion and displayed diminished IL-22 level in kidney. Prevented BP elevation markedly and diminished urinary albumin/creatinine ratio, BUN and Scr. Repressed the expression of IL-1β, IL-6, TNF-α, α-SMA, FN and Col I and diminished the extent of fibrosis.

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Animal/Disease Models: C57BL/6 mice[1]
Doses: 20 μM
Route of Administration: 20 μM; for 3 h
Experimental Results: Downregulated renal CCL20, CCL22 and CCL27 concentrations.

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Ang II-induced hypertensive rat model: Use male Sprague-Dawley rats (200-220 g). Implant osmotic minipumps subcutaneously to infuse Ang II (400 ng/kg/min) for 4 weeks. From the first day of Ang II infusion, administer Irbesartan (SR-47436; BMS-186295) (30 mg/kg/day) by oral gavage (dissolved in 0.5% carboxymethyl cellulose) for 4 weeks. Measure SBP weekly using tail-cuff plethysmography. At the end of the experiment, collect blood to detect Scr and BUN, collect 24-hour urine to measure protein excretion, and harvest renal tissues for immunohistochemical staining (to count Th22 cells) [3]

Absorption, Distribution and Excretion
Irbesartan has a bioavailability of 60-80% and a time to peak concentration (Tmax) of 1.5-2 hours. Co-administration with food does not affect the bioavailability of irbesartan. In one study, healthy subjects received single or multiple oral doses of 150 mg, 300 mg, 600 mg, and 900 mg of irbesartan. The AUC of a single 150 mg dose was 9.7 ± 3.0 µg•hr/mL, Tmax was 1.5 hours, half-life was 16 ± 7 hours, and Cmax was 1.9 ± 0.4 µg/mL. After a single 300 mg dose, the AUC was 20.0 ± 5.2 µg•hr/mL, Tmax was 1.5 hours, half-life was 14 ± 7 hours, and Cmax was 2.9 ± 0.9 µg/mL. After a single 600 mg dose, the AUC was 32.6 ± 11.9 µg•hr/mL, Tmax was 1.5 hours, half-life was 14 ± 8 hours, and Cmax was 4.9 ± 1.2 µg/mL. After a single 900 mg dose, the AUC was 44.8 ± 20.0 µg•hr/mL, Tmax was 1.5 hours, half-life was 17 ± 7 hours, and Cmax was 5.3 ± 1.9 µg/mL. After multiple 150 mg doses, the AUC was 9.3 ± 3.0 µg•hr/mL, Tmax was 1.5 hours, half-life was 11 ± 4 hours, and Cmax was 2.04 ± 0.4 µg/mL. After multiple 300 mg doses, the AUC was 19.8 ± 5.8 µg·hr/mL, Tmax was 2.0 hours, half-life was 11 ± 5 hours, and Cmax was 3.3 ± 0.8 µg/mL. After multiple 600 mg doses, the AUC was 31.9 ± 9.7 µg·hr/mL, Tmax was 1.5 hours, half-life was 15 ± 7 hours, and Cmax was 4.4 ± 0.7 µg/mL. After multiple 900 mg doses, the AUC was 34.2 ± 9.3 µg·hr/mL, Tmax was 1.8 hours, half-life was 14 ± 6 hours, and Cmax was 5.6 ± 2.1 µg/mL. 20% of the radiolabeled irbesartan oral dose is excreted in the urine, and the remainder in the feces. <2% of the dose is excreted unchanged in the urine. The volume of distribution of irbesartan is 53-93 L. Irbesartan has a total plasma clearance of 157-176 mL/min and a renal clearance of 3.0-3.5 mL/min. Irbesartan is an orally active drug that exerts its activity without biotransformation. It is rapidly and completely absorbed orally, with a mean absolute bioavailability of 60% to 80%. Peak plasma concentrations of irbesartan are reached 1.5 to 2 hours after oral administration of avapro. Food does not affect the bioavailability of avapro. Irbesartan exhibits linear pharmacokinetic characteristics within the therapeutic dose range. The terminal elimination half-life of irbesartan is, on average, 11 to 15 hours. Steady-state plasma concentrations are reached within 3 days. With repeated once-daily dosing, the accumulation of irbesartan in plasma is limited (<20%). Animal studies have shown that radiolabeled irbesartan can weakly cross the blood-brain barrier and placenta. Irbesartan binds 90% to serum proteins (primarily albumin and α1-acid glycoprotein), with negligible binding to blood cell components. The mean volume of distribution is 53 to 93 liters. Total plasma clearance and renal clearance are 157 to 176 mL/min and 3.0 to 3.5 mL/min, respectively. Irbesartan accumulation after repeated administration is not clinically significant. It is unclear whether irbesartan is secreted into human milk, but irbesartan or some of its metabolites are secreted in low concentrations into the milk of lactating rats. Metabolism/Metabolites: Irbesartan is primarily metabolized in the liver via glucuronidation and oxidation. Most metabolism occurs through the action of CYP2C9, with negligible action by CYP3A4. Some hydroxylation also occurs during the metabolism of irbesartan. Irbesartan can be metabolized via UGT1A3 glucuronidation to generate metabolite M8, oxidized to generate metabolite M3, or via CYP2C9 hydroxylation to generate one of metabolites M4, M5, or M7. Metabolites M4, M5, and M7 can all be hydroxylated to generate metabolite M1, which is then oxidized to generate metabolite M2. The M4 metabolite can also be oxidized to generate metabolite M6, followed by hydroxylation to generate metabolite M2. Finally, irbesartan can also generate a small amount of metabolite SR 49498 via an unknown mechanism. Irbesartan is primarily metabolized via glucuronidation and oxidation. Following oral or intravenous administration of 14C-labeled irbesartan, over 80% of the radioactivity in circulating plasma is attributed to unmetabolized irbesartan. The major circulating metabolite of irbesartan is the inactive irbesartan glucuronide conjugate (approximately 6%). The remaining oxidative metabolites have minimal effect on the pharmacological activity of irbesartan. Irbesartan and its metabolites are primarily excreted via bile and kidneys. Following oral or intravenous administration of 14C-labeled irbesartan, approximately 20% of the radioactive material is excreted in the urine as irbesartan or irbesartan glucuronide, with the remainder excreted in the feces. In vitro studies have shown that the oxidation of irbesartan by cytochrome P450 isoenzymes is primarily mediated by 2C9, with negligible metabolic activity by 3A4. Irbesartan is neither metabolized by drug-related isoenzymes (1A1, 1A2, 2A6, 2B6, 2D6, 2E1) nor significantly induced or inhibited by these isoenzymes. No induction or inhibition of 3A4 was observed.
The known metabolites of irbesartan include M7, (1S,4S,5S,6R)-3-[5-[2-[4-[(2-butyl-4-oxo-1,3-diazaspiro[4.4]non-1-en-3-yl)methyl]phenyl]phenyl]-5H-tetrazol-2-onthiol-2-yl]-2,4,5,6-tetrahydroxycyclohexane-1-carboxylic acid, M3, and 2-(3-hydroxybutyl)-3-({4-[2-(2H-1,2,3,4-tetrazol-5-yl)phenyl]phenyl}methyl)-1,3-diazaspiro[4.4]non-1-en-4-one.

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Biological half-life
The terminal elimination half-life of irbesartan is 11–15 hours. The terminal elimination half-life of irbesartan is on average 11 to 15 hours.

Toxicity Summary
Identification and Uses: Irbesartan crystals are formulated as oral tablets. Irbesartan is an angiotensin II type 1 (AT1) receptor antagonist. It can be used alone or in combination with other classes of antihypertensive drugs to treat hypertension. It is also used to treat diabetic nephropathy in patients with type 2 diabetes and hypertension. Human Exposure and Toxicity: The most likely manifestations of irbesartan overdose include hypotension and tachycardia; overdose may also cause bradycardia. Irbesartan is contraindicated during pregnancy. While use in early pregnancy does not indicate a risk of serious malformations, use in mid-to-late pregnancy may lead to teratogenicity and serious fetal and neonatal toxicity. Fetal toxicity may include anuria, oligohydramnios, fetal craniofacial dysplasia, intrauterine growth restriction, preterm birth, and patent ductus arteriosus. Anuria-associated oligohydramnios may lead to fetal limb contractures, craniofacial malformations, and pulmonary dysplasia. Neonates exposed to irbesartan in utero may develop severe anuria and hypotension unresponsive to vasopressors and volume expansion therapy. Animal studies: No carcinogenicity of irbesartan was observed during a 2-year administration period in rats or mice. Furthermore, irbesartan administration had no effect on fertility or mating behavior in male and female rats. When pregnant rats were treated with the drug from day 0 to day 20 of gestation, even at doses as low as 50 mg/kg/day, the incidence of fetal cavitation, hydroureter, and/or renal papillary absence was increased. Subcutaneous edema was observed in fetuses even at doses as low as 180 mg/kg/day. Since these abnormalities were not observed in rats treated with the drug from day 6 to day 15 of gestation, these abnormalities appear to reflect the late-pregnancy effects of the drug. In pregnant rabbits, oral administration of irbesartan at 30 mg/kg/day was associated with maternal mortality and abortion. Surviving female rabbits receiving this dose showed a slightly increased early embryonic resorption rate and a correspondingly reduced number of live fetuses. Irbesartan did not show mutagenicity in a series of in vitro tests (Ames microbial assay, rat hepatocyte DNA repair assay, V79 mammalian cell forward mutation assay). Irbesartan was negative in multiple chromosomal aberration induction assays (in vitro human lymphocyte assay; in vivo mouse micronucleus assay).

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Hepatotoxicity
Irbesartan was associated with a low incidence of elevated serum transaminases (
Probability score: C (likely a rare cause of clinically significant liver injury)).

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Use during pregnancy and lactation
◉ Overview of use during lactation
Since there is no information on the use of irbesartan during lactation, alternative medications are recommended, especially for breastfed newborns or preterm infants.
◉ Effects on breastfed infants
No relevant published information found as of the revision date.
◉ Effects on lactation and breast milk
No relevant published information found as of the revision date. Date. Protein Binding Irbesartan has a 90% protein binding rate in plasma, primarily binding to albumin and α1-acid glycoprotein. Interactions Alisartan is contraindicated in diabetic patients when used in combination with avapro. Patients with renal insufficiency (glomerular filtration rate <60 mL/min) should avoid using alisartan in combination with avapro. Compared to monotherapy, the use of angiotensin receptor blockers, ACE inhibitors, or dual blocking of the renin-angiotensin system (RAS) with alisartan increases the risk of hypotension, hyperkalemia, and altered renal function (including acute renal failure). Patients taking avapro and other medications affecting the RAS should be closely monitored for blood pressure, renal function, and electrolytes. Concomitant use of potassium-sparing diuretics, potassium supplements, or potassium-containing salt substitutes may lead to elevated serum potassium levels. Irbesartan metabolism may be reduced when used in combination with tolbutamide. For more complete data on irbesartan interactions (6 items in total), please visit the HSDB record page.

[1]. Schupp M, et al. Angiotensin type 1 receptor blockers induce peroxisome proliferator-activated receptor-gamma activity. Circulation. 2004 May 4;109(17):2054-7. Epub 2004 Apr 26.
[2]. Ruiz E, et al. Importance of intracellular angiotensin II in vascular smooth muscle cell apoptosis: inhibition by the angiotensin AT1 receptor antagonist irbesartan. Eur J Pharmacol. 2007 Jul 19;567(3):231-9. Epub 2007 Apr 6.
[3]. Yong Zhong, et al. Irbesartan may relieve renal injury by suppressing Th22 cells chemotaxis and infiltration in Ang II-induced hypertension. Int Immunopharmacol

Therapeutic Uses

Angiotensin II type 1 receptor blocker; antihypertensive drug
Avapro (irbesartan) is indicated for the treatment of hypertension. It can be used alone or in combination with other antihypertensive drugs. /Included on US product label/
Avapro is indicated for the treatment of diabetic nephropathy in patients with type 2 diabetes and hypertension who have elevated serum creatinine and proteinuria (>300 mg/day). In these patients, Avapro can slow the progression of kidney disease, as measured by the doubling of serum creatinine or the incidence of end-stage renal disease (requiring dialysis or kidney transplantation). /Included on US product label/
Angiotensin II receptor antagonists (including irbesartan) have been used to treat congestive heart failure. /Not included on US product label/
Drug Warnings
/Black Box Warning/ Warning: Fetal toxicity. Avapro should be discontinued as soon as pregnancy is discovered. Drugs that act directly on the renin-angiotensin system may cause harm or even death to the developing fetus.
Use of medications acting on the renin-angiotensin system in the mid-to-late stages of pregnancy can reduce fetal kidney function and increase fetal and neonatal morbidity and mortality. The resulting oligohydramnios may be associated with fetal lung malformation and skeletal deformities. Potential neonatal adverse reactions include craniosynostosis, anuria, hypotension, renal failure, and death. Avapro should be discontinued as soon as pregnancy is confirmed. These adverse consequences are usually associated with the use of such medications in the mid-to-late stages of pregnancy. Most epidemiological studies investigating fetal malformations following early pregnancy use of antihypertensive drugs have not differentiated between medications affecting the renin-angiotensin system and other antihypertensive drugs. Appropriate management of maternal hypertension during pregnancy is crucial for optimizing maternal and infant outcomes. In rare cases where no suitable alternative medication is available for a particular patient, and medications affecting the renin-angiotensin system must be used, the pregnant woman should be informed of the potential risks to the fetus. A series of ultrasound examinations should be performed to assess the amniotic environment. If oligohydramnios is detected, avapro should be discontinued unless discontinuation is a life-saving measure for the pregnant woman. Fetal monitoring may be required depending on gestational age. However, patients and physicians should note that oligohydramnios may only occur after irreversible damage to the fetus. Newborns with intrauterine exposure to avaprost: If oliguria or hypotension occurs, focus should be placed on maintaining blood pressure and renal perfusion. Exchange transfusion or dialysis may be necessary to reverse hypotension and/or replace impaired kidney function. FDA Pregnancy Risk Classification: D/Clear evidence of risk. Fetal risk has been confirmed by human studies, trial data, or post-marketing data. Nevertheless, the potential benefits of using this drug may outweigh the potential risks. For example, this drug may be acceptable in life-threatening situations or when a safer drug is unavailable or ineffective. / For more complete data on drug warnings for irbesartan (16 of them), please visit the HSDB record page.

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Pharmacodynamics
Irbesartan is an angiotensin receptor blocker used to treat hypertension and diabetic nephropathy.
Because it is usually taken once a day, it has a long duration of action and a wide therapeutic index, with doses as low as 150 mg per day, but healthy subjects tolerated doses of up to 900 mg per day well. Irbesartan (SR-47436; BMS-186295) has a dual action: it is both an AT1R antagonist and a partial agonist of PPAR-γ, which may contribute to its other beneficial effects beyond lowering blood pressure (e.g., anti-inflammatory and metabolic regulation) [1] - The mechanism by which irbesartan (SR-47436; BMS-186295) inhibits VSMC apoptosis involves blocking a pro-apoptotic signaling pathway activated by intracellular Ang II, rather than just extracellular Ang II [2] - Irbesartan (SR-47436; BMS-186295) alleviates kidney damage in hypertensive rats. It reduces kidney inflammation and tissue damage by inhibiting the chemotaxis and infiltration of Th22 cells [3]

C25H28N6O

428.53

428.232

C, 70.07; H, 6.59; N, 19.61; O, 3.73

138402-11-6

Irbesartan-d4;1216883-23-6;Irbesartan hydrochloride;329055-23-4;Irbesartan-d6;Irbesartan-d6-1;2375621-21-7

3749

White to off-white solid

1.3±0.1 g/cm3

648.6±65.0 °C at 760 mmHg

180-181°C

346.0±34.3 °C

0.0±1.9 mmHg at 25°C

1.690

4.51

1

5

7

32

682

0

O=C1C2(C([H])([H])C([H])([H])C([H])([H])C2([H])[H])N=C(C([H])([H])C([H])([H])C([H])([H])C([H])([H])[H])N1C([H])([H])C1C([H])=C([H])C(C2=C([H])C([H])=C([H])C([H])=C2C2N=NN([H])N=2)=C([H])C=1[H]

YOSHYTLCDANDAN-UHFFFAOYSA-N

InChI=1S/C25H28N6O/c1-2-3-10-22-26-25(15-6-7-16-25)24(32)31(22)17-18-11-13-19(14-12-18)20-8-4-5-9-21(20)23-27-29-30-28-23/h4-5,8-9,11-14H,2-3,6-7,10,15-17H2,1H3,(H,27,28,29,30)

2-butyl-3-[[4-[2-(2H-tetrazol-5-yl)phenyl]phenyl]methyl]-1,3-diazaspiro[4.4]non-1-en-4-one

2934.99.03.00

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)

Solubility in Formulation 1: ≥ 2.5 mg/mL (5.83 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 (5.83 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 (5.83 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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Solubility in Formulation 4: 30% PEG400+0.5% Tween80+5% Propylene glycol : 30 mg/mL

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