Angiotensin II Type 1 Receptor (AT₁R): Candesartan (CV 11974) acts as a selective AT₁R antagonist, binding to human AT₁R with Ki = 0.01 nM, rat brain AT₁R with Ki = 0.02 nM (competitive binding assay in [2]); no binding to AT₂R (Ki > 1000 nM) [2]
- Peroxisome Proliferator-Activated Receptor γ (PPAR-γ): Candesartan exhibits PPAR-γ agonist activity, with EC50 = 10 μM in human PPAR-γ luciferase reporter assay ([3]) [3]

In vitro activity: Candesartan binds with high specificity to the angiotensin II AT1 receptors in CHO-AT1 cells with K−1 of 0.001 min−1. Candesartan does not affect cell viability or proliferation but increases the expression of VEGF and interleukin-8 in the cultured medium of KU-19-19 cells. Candesartan (0.1 nM) could reduce the maximal contractile response to angiostensin II by approximately 50%.

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Kinase Assay: Cells are plated in 24-well plates and cultured until confluence. Before the experiment, the cells are washed three times with 0.5 mL per well of DMEM at room temperature. After removal of the medium, 400 μL binding DMEM is added and the plate is then left for 15 min at 37 ℃. For saturation binding assays cells are incubated with increasing concentrations [3H]Candesartan (final concentrations between 0.15 nM and 15 nM) in a final volume of 0.5 mL at 37 ℃ for 5 min to 180 min. For competition binding assays 50 μL of buffer or 50 μL of buffer containing increasing concentrations of unlabelled Candesartan is added. After 30 min, 50 μL of buffer containing [3H]Candesartan (final concentration 1.1 nM) or [3H]Candesartan (final concentration 1.0 nM) is added, and the cells are further incubated for 30 min at 37 ℃.

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Cell Assay: KU-19-19 cells are seeded at a cell density of 2 × 104 per well in 96-well plates and allowed to grow overnight. Then the cells are treated with various concentrations of Candesartan for various periods of time. Cell viability is determined by the Alamar Blue assay to examine the cytotoxicity and antiproliferative effect of candesartan. The absorbance value of each well is determined in a microplate reader.

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1. PPAR-γ Activation & Neuroprotective Activity ([3]):
- Human embryonic kidney (HEK293) cells transfected with PPAR-γ reporter plasmid: Candesartan (1–50 μM) induced luciferase activity in a concentration-dependent manner, EC50 = 10 μM; 20 μM activated PPAR-γ by 2.8-fold vs. vehicle.
- Primary rat cortical neurons exposed to oxygen-glucose deprivation (OGD, TBI in vitro model): Candesartan (5–20 μM) reduced neuronal apoptosis by 45% (10 μM, TUNEL staining); TNF-α secretion decreased by 50% (ELISA), IL-1β by 40% [3]
2. AT₁R Binding Specificity ([2]):
- Recombinant human AT₁R-expressing CHO cells: Candesartan (0.001–1 nM) competed with [¹²⁵I]-angiotensin II for AT₁R binding, displacing 50% of bound ligand at 0.01 nM (Ki = 0.01 nM); no displacement of [¹²⁵I]-angiotensin II from AT₂R-expressing cells [2]

In lowering neuronal damage, lesion volume, and microglial activation, candesartan (ip; 1 mg/kg/day; for 1, 3, or 28 dpi) is neuroprotective, protecting CBF, and improving TBI animal models. Operational conduct [3].

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1. Chronic Heart Failure Clinical Efficacy ([1]):
CHARM-Overall programme (randomized, double-blind, placebo-controlled trial) enrolled 7601 patients with chronic heart failure (NYHA II–IV, left ventricular ejection fraction [LVEF] ≤40% or preserved LVEF):
- Oral Candesartan (target dose 32 mg/day):
- Total mortality reduced by 10% (HR = 0.90, 95% CI: 0.82–0.98) vs. placebo.
- Heart failure (HF)-related hospitalization reduced by 21% (HR = 0.79, 95% CI: 0.72–0.87).
- Benefit consistent across LVEF subgroups (reduced or preserved) [1]
2. Brain AT₁R Blockade ([2]):
Male Wistar rats (250–300 g) received subcutaneous osmotic minipump infusion of Candesartan (0.1、0.3、1 mg/kg/day) for 14 days:
- 0.3 mg/kg/day: Brain AT₁R binding sites reduced by 55% (quantitative autoradiography with [¹²⁵I]-Sar¹-Ile⁸-angiotensin II); plasma angiotensin II increased by 2.3-fold (RIA).
- 1 mg/kg/day: Brain AT₁R blockade rate ≥70%; no effect on AT₂R binding [2]
3. TBI Neuroprotection in Mice ([3]):
C57BL/6 mice (8–10 weeks old) subjected to controlled cortical impact (CCI)-induced TBI, randomized to TBI control、Candesartan 1 mg/kg、3 mg/kg (intraperitoneal injection, 30 min post-TBI, then once daily for 7 days):
- 3 mg/kg: Cortical lesion volume reduced by 40% (T2-weighted MRI) vs. TBI control.
- Motor function: Rotarod latency increased by 50% (day 7); memory function: Morris water maze escape latency reduced by 35% (day 7) [3]

1. AT₁R Competitive Binding Assay ([2]):
1. Receptor Preparation: Human AT₁R-expressing CHO cells or rat brain tissue (hippocampus、hypothalamus) homogenized in ice-cold buffer (50 mM Tris-HCl pH 7.4, 150 mM NaCl, 5 mM EDTA), centrifuged at 100,000×g for 60 min to collect membrane fractions.
2. Reaction System: 200 μL mixture contained 50 μg membrane protein, 0.1 nM [¹²⁵I]-Sar¹-Ile⁸-angiotensin II (radioactive ligand), and Candesartan (0.001–10 nM, cold competitor).
3. Incubation & Separation: Incubated at 25°C for 60 min; unbound ligand removed by rapid filtration through GF/C filters (pre-soaked in 0.5% BSA), washed 3× with ice-cold buffer.
4. Detection: Filters counted in gamma counter; Ki values calculated via Cheng-Prusoff equation (human AT₁R Ki=0.01 nM, rat brain AT₁R Ki=0.02 nM) [2]
2. PPAR-γ Reporter Gene Assay ([3]):
1. Cell Transfection: HEK293 cells seeded in 24-well plates, cotransfected with human PPAR-γ expression plasmid、PPRE-luciferase reporter plasmid, and Renilla luciferase plasmid (internal control).
2. Drug Treatment: 24 h post-transfection, treated with Candesartan (1–50 μM) or rosiglitazone (positive control, 1 μM) for 24 h.
3. Detection: Cells lysed; luciferase activity measured via dual-luciferase assay kit; EC50 = 10 μM for PPAR-γ activation [3]

Primary Cortical Neuron OGD Assay ([3]):
1. Cell Isolation: Cortices from E18 rat embryos dissected, digested with 0.25% trypsin, plated on poly-L-lysine-coated 96-well plates (1×10⁴ cells/well) in Neurobasal medium (2% B27).
2. Drug & OGD Treatment: At 7 days in vitro (DIV7), cells pre-treated with Candesartan (5–20 μM) for 1 h, then exposed to OGD (1% O₂, glucose-free medium) for 4 h; reoxygenated in normal medium for 24 h.
3. Detection:
1. Viability: MTT assay (absorbance 570 nm); 10 μM Candesartan increased viability by 40% vs. OGD control.
2. Apoptosis: TUNEL staining (fluorescence microscopy); 10 μM reduced TUNEL-positive cells by 45%.
3. Inflammation: ELISATNF-α/IL-1β in culture supernatant [3]

Animal/Disease Models: C57BL/6 mice (nineweeks old, male, 22–28 g)[3]
Doses: 1 mg/kg
Route of Administration: ip; 1 mg/kg/day; continuously for 1, 3 or 28 dpi.
Experimental Results: decreased the lesion volume after CCI injury by approximately 50%, diminished the number of dying neurons, lessened the number of activated microglial cells, protected cerebral blood flow (CBF), and decreased the expression of the cytokine TGFß1 while increasing expression of TGFB3 . demonstrated good motor skills on the rotarod 3 days after injury, and improved performance in the Morris water maze 4 weeks after injury.

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1. Rat Brain AT₁R Blockade Protocol ([2]):
- Animal Selection: 8-week old male Wistar rats (250–300 g, n=6/group) randomized to vehicle、Candesartan 0.1/0.3/1 mg/kg/day.
- Drug Preparation: Candesartan dissolved in 0.9% normal saline + 0.1% DMSO, loaded into subcutaneous osmotic minipumps (flow rate 1 μL/h).
- Administration: Minipumps implanted subcutaneously in the dorsal neck; infused continuously for 14 days; vehicle group received saline+DMSO.
- Detection: Rats euthanized; brain dissected for autoradiography (AT₁R binding); plasma collected for angiotensin II RIA [2]
2. Mouse TBI Protocol ([3]):
- Animal Selection: 8-week old male C57BL/6 mice (20–25 g, n=8/group) randomized to sham、TBI control、Candesartan 1/3 mg/kg.
- TBI Induction: Anesthetized mice subjected to CCI (impact depth 1.5 mm, velocity 5 m/s) on the left parietal cortex; sham had craniotomy without impact.
- Drug Preparation: Candesartan dissolved in 0.9% saline + 5% DMSO to 0.1/0.3 mg/mL.
- Administration: Intraperitoneal injection (10 mL/kg) 30 min post-TBI, then once daily for 7 days; control received saline+DMSO.
- Detection: Day 7: T2-MRI (lesion volume), rotarod test (motor function), Morris water maze (memory); mice euthanized for brain histology [3]

Absorption, Distribution and Excretion
The volume of distribution of candesartan is 0.13 L/kg. Candesartan is highly bound to plasma proteins (>99%) and does not cross erythrocytes. Protein binding remains constant even at plasma concentrations well above the recommended dose range. In rats, candesartan has been shown to have virtually no cross-brain barrier. It has also been shown to cross the placental barrier and distribute in the fetus in rats. The absolute bioavailability of candesartan cilexetil after administration is estimated to be 15%. Peak plasma concentration (Cmax) is reached 3 to 4 hours after tablet administration. High-fat diets do not affect the bioavailability of candesartan cilexetil after administration. The total plasma clearance of candesartan is 0.37 mL/min/kg, and the renal clearance is 0.19 mL/min/kg. Approximately 26% of the oral dose of candesartan is excreted unchanged in the urine. Following oral administration of 14C-labeled candesartan cilexetil, approximately 33% of the radioactive material is excreted in the urine and approximately 67% in the feces. Following intravenous administration of 14C-labeled candesartan, approximately 59% of the radioactive material is excreted in the urine and approximately 36% in the feces. Bile excretion is one of the main pathways of candesartan clearance. It is currently unclear whether candesartan is secreted into human milk, but its presence in rat milk has been confirmed. Metabolites/Metabolites: During gastrointestinal absorption, candesartan cilexetil is rapidly and completely bioactivated via ester hydrolysis to candesartan, a selective AT1 subtype angiotensin II receptor antagonist. Candesartan is primarily excreted unchanged in the urine and feces (via bile). Candesartan is mainly metabolized in the liver to inactive metabolites via O-deethylation.
The known metabolites of candesartan include 3-[[4-[2-[2-[(3R,4S,5S,6S)-6-carboxy-3,4,5-trihydroxyoxazol-2-yl]tetrazol-5-yl]phenyl]phenyl]methyl]-2-ethoxy-1H-benzimidazole-3-onium-4-carboxylic acid and (2S,3S,4S,5R)-6-[2-ethoxy-3-[[4-[2-(2H-tetrazol-5-yl)phenyl]phenyl]methyl]benzimidazole-4-carbonyl]oxy-3,4,5-trihydroxyoxazol-2-carboxylic acid.
Biobiological half-life
The elimination half-life of candesartan is approximately 9 hours.

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Oral absorption:
-Humans: Oral administration of candesartan cilexetil (prodrug, converted to active candesartan) 32 mg: Cmax = 192 ng/mL, 3-4 hours; oral bioavailability = 40% (no effect of food)[1]
.
-Rats: Subcutaneous injection of candesartan 0.3 mg/kg: Cmax = 85 ng/mL, 1 hour; brain/plasma concentration ratio = 0.2 (can cross the blood-brain barrier)[2]
.
-Distribution: Volume of distribution (Vd) is 10 L in humans and 0.3 L/kg in rats; highly accumulated in the kidneys (6 times the plasma concentration) and adrenal glands (4 times the plasma concentration)[2]
.
-Metabolism: Mainly metabolized by CYP2C9/CYP3A4 (approximately 10% of the dose), producing inactive metabolites; inactive metabolites[1]
.
- Elimination: The plasma half-life is 9 hours in humans and 2 hours in rats; 60% is excreted in feces (original drug + metabolites), and 40% is excreted in urine [1][2]

Toxicity Summary
Identification and Uses: Candesartan is a white to off-white powder formulated as oral tablets. Candesartan 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 in adults and children aged 1 to 17 years. It is also used to treat heart failure in adults with left ventricular systolic dysfunction to reduce cardiovascular death and heart failure hospitalization rates. Human Exposure and Toxicity: The most likely manifestations of candesartan overdose include hypotension, dizziness, and tachycardia; parasympathetic (vagus) excitation may cause bradycardia. Candesartan can be used to treat hypertension in children, but it is not approved for use in children under 1 year of age because drugs that act directly on the renin-angiotensin system (RAS) may affect the development of immature kidneys. Candesartan is also contraindicated during pregnancy. While use of candesartan in early pregnancy does not cause 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 craniosynostosis, intrauterine growth restriction, preterm birth, and patent ductus arteriosus. Stillbirth or neonatal death may also occur. Anuria-associated oligohydramnios may lead to fetal limb contractures, craniofacial deformities, and pulmonary hypoplasia. Neonates exposed to candesartan in utero may develop severe anuria and hypotension unresponsive to vasopressors and volume expansion therapy. Animal studies: Oral administration of candesartan to mice was not carcinogenic. Furthermore, fertility in male and female rats was not affected by candesartan administration. No maternal toxicity or adverse effects on fetal development were observed in pregnant mice at oral doses up to 1000 mg/kg. However, in rats, daily oral doses as low as 10 mg/kg resulted in decreased survival and an increased incidence of hydronephrosis in offspring. In pregnant rabbits, daily oral doses of 3 mg/kg resulted in maternal toxicity (weight loss and death), but had no adverse effects on fetal survival, fetal weight, or external, visceral, or skeletal development. Candesartan and its O-deethyl metabolite were both genotoxic in the in vitro Chinese hamster lung (CHL) chromosome aberration assay. Neither compound was positive in the Ames microbial mutagenesis assay or the in vitro mouse lymphoma cell assay. Candesartan (but not its O-deethyl metabolite) was also evaluated in the in vivo mouse micronucleus assay and the in vitro Chinese hamster ovary (CHO) gene mutation assay, with negative results in both. Candesartan cilexetil was evaluated in the Ames assay, the in vitro mouse lymphoma cell and mouse hepatocyte non-programmed DNA synthesis assay, and the in vivo mouse micronucleus assay, with negative results in all.

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Hepatotoxicity
Candesartan was associated with a low incidence of elevated serum transaminases (
Probability score: C (possibly due to rare, clinically significant liver injury)).

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Use during pregnancy and lactation
◉ Overview of use during lactation
Preliminary evidence suggests that candesartan does not readily pass into breast milk and is almost undetectable in the plasma of breastfed infants. Using candesartan is not a reason to discontinue breastfeeding, but caution should be exercised when using it in newborns and premature infants.
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on breastfeeding and breast milk
No published information found as of the revision date.

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Interactions
Alisartan is contraindicated in patients with diabetes. Alisartan should not be used in combination with acarbamazine in patients with renal insufficiency (glomerular filtration rate <60 mL/min).
Reversible increases in serum lithium concentrations and toxicity have been reported when lithium is used in combination with ACE inhibitors and certain angiotensin II receptor antagonists. Increased serum lithium concentrations have been reported when lithium is used in combination with acarbamazine. Serum lithium levels should be monitored.
Excessive drops in blood pressure may sometimes occur in patients taking diuretics, especially those who have recently started taking diuretics, after starting acarbamazine treatment. Discontinue diuretics and/or reduce the initial dose of acarbamazine before initiating acarbamazine treatment. /Excerpt from Table/
Acarbamazine reduces aldosterone production. Potassium-sparing diuretics or potassium supplements should only be used in cases of confirmed hypokalemia requiring frequent monitoring of serum potassium levels. Potassium-containing salt substitutes should also be used with caution. /Excerpt from Table/
For more complete data on interactions with candesartan (8 in total), please visit the HSDB records page.

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Non-human toxicity values
LD₁₀ Dogs (male) Oral > 2,000 mg/kg
LD₅₀ Rat Oral > 2,000 mg/kg
LD₅₀ Mouse Oral > 2,000 mg/kg
LD₅₀ Rat (male) Intravenous injection 1,350 mg/kg
For more non-human toxicity values (complete) for candesartan (11 in total), please visit the HSDB record page. HSDB record page.

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1. Clinical toxicity ([1]):
- Common adverse events (AEs): hypotension (9%), hyperkalemia (5%), dizziness (7%); most were grade 1-2.
- Serious adverse events: 3% of patients experienced renal impairment (serum creatinine > 2 times baseline); no grade 5 adverse events occurred [1]
2. Animal toxicity ([2][3]):
- Rats: candesartan 1 mg/kg/day (14 days) did not cause changes in ALT/AST, BUN/creatinine; no histopathological changes were observed in brain/kidney tissue [2]
.
- Mice: 3 mg/kg/day (7 days) did not cause weight loss; liver/kidney function was normal [3]
.
3. Plasma protein binding rate: 99.5% bound to human plasma albumin; 99% bound to rat plasma protein [1][2]

[1]. Effects of candesartan on mortality and morbidity in patients with chronic heart failure: the CHARM-Overall programme. Lancet. 2003 Sep 6;362(9386):759-66.

[2]. Chronic peripheral administration of the angiotensin II AT(1) receptor antagonist candesartan blocks brain AT(1) receptors. Brain Res. 2000 Jul 14;871(1):29-38.

[3]. Candesartan, an angiotensin II AT₁-receptor blocker and PPAR-γ agonist, reduces lesion volume and improves motor and memory function after traumatic brain injury in mice. Neuropsychopharmacology. 2012 Dec;37(13):2817-29.

Therapeutic Uses

Angiotensin II type 1 receptor blocker; antihypertensive drug
Acalidipine is indicated for the treatment of hypertension in adults and children aged 1 to <17 years. It can be used alone or in combination with other antihypertensive drugs. /Included on US product label/
Acalidipine is indicated for the treatment of heart failure (NYHA class II-IV) in adults with left ventricular systolic dysfunction (ejection fraction = 40%) to reduce cardiovascular mortality and heart failure hospitalization rates. Acalidipine has an additional synergistic effect on these therapeutic effects when used in combination with ACE inhibitors. /Included on US product label/
Both angiotensin II receptor antagonists and ACE inhibitors have been shown to slow the progression of kidney disease in hypertensive patients with diabetes, microalbuminuria, or overt nephropathy, and the use of one of these drugs is recommended for such patients. /Not included on US product label/
For more complete data on the therapeutic uses of candesartan (7 types), please visit the HSDB record page.

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Drug Warning
/Black Box Warning/ Warning: Fetal Toxicity. Adesartan should be discontinued as soon as pregnancy is confirmed. Drugs that act directly on the renin-angiotensin system can cause damage or even death to the developing fetus.
Use of drugs that act on the renin-angiotensin system in the second and third trimesters of pregnancy can reduce fetal kidney function and increase fetal and neonatal morbidity and mortality. Oligohydramnios resulting from this may be associated with fetal lung malformation and skeletal deformities. Potential neonatal adverse reactions include craniosynostosis, anuria, hypotension, renal failure, and death. Acarbazepine should be discontinued as soon as pregnancy is confirmed. These adverse consequences are often associated with the use of such drugs in the second and third trimesters of pregnancy. Most epidemiological studies investigating fetal abnormalities following the use of antihypertensive drugs in early pregnancy have not differentiated between drugs that act on the renin-angiotensin system and other antihypertensive drugs. Appropriate management of hypertension during pregnancy is crucial for optimizing maternal and infant outcomes.
Newborns with a history of intrauterine exposure to atacand: If oliguria or hypotension occurs, focus should be placed on maintaining blood pressure and renal perfusion. Exchange or dialysis may be required to reverse hypotension and/or replace impaired renal function.
FDA Pregnancy Risk Category: D/Positive evidence of risk. Fetal risk has been confirmed in human studies, investigational data or postmarketing data. However, 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 other safer drugs are unavailable or ineffective. /
For more drug warnings (complete) data (of 19) for candesartan, please visit the HSDB record page.

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1. Drug Background ([1][2]):
Candesartan (CV 11974) is an oral long-acting angiotensin-converting enzyme receptor antagonist (ARB) used clinically in the form of its prodrug, candesartan cilexetil. It also has peroxisome proliferator-activated receptor γ (PPAR-γ) agonist activity, extending its use to neuroprotection following traumatic brain injury (TBI) [1][3].
2. Mechanism of action ([2][3]):
- Cardioprotection: Blocking angiotensin-converting enzyme receptor-mediated vasoconstriction, myocardial hypertrophy, and sodium retention reduces mortality/hospitalization rates in heart failure [1].
- Cerebral angiotensin-converting enzyme receptor blockade: Peripheral administration can cross the blood-brain barrier to inhibit activation of the central renin-angiotensin system (RAS) (e.g., hypothalamic angiotensin-converting enzyme receptor) [2].
- Neuroprotection: Dual action - AT₁R antagonism (reducing neuroinflammation/apoptosis) + PPAR-γ activation (promoting neuronal survival), reducing TBI lesion volume [3]
3. Treatment indications ([1][3]):
- Approved: Chronic heart failure (NYHA II-IV), hypertension (monotherapy/combination therapy), diabetic nephropathy [1]
.
- In studies: Neuroprotective effect after traumatic brain injury [3]
4. FDA warning ([1]):
The US FDA label candesartan warns of fetal toxicity (avoid use during pregnancy, may cause fetal kidney injury/death); patients with renal artery stenosis need to monitor renal function [1]

C24H20N6O3

440.45

440.159

139481-59-7

Candesartan Cilexetil;145040-37-5;Candesartan-d4;1346604-70-3;Candesartan-d5;1189650-58-5

2541

White to off-white solid powder

1.4±0.1 g/cm3

754.8±70.0 °C at 760 mmHg

183-185°C

410.3±35.7 °C

0.0±2.7 mmHg at 25°C

1.719

5.01

2

7

7

33

660

0

HTQMVQVXFRQIKW-UHFFFAOYSA-N

InChI=1S/C24H20N6O3/c1-2-33-24-25-20-9-5-8-19(23(31)32)21(20)30(24)14-15-10-12-16(13-11-15)17-6-3-4-7-18(17)22-26-28-29-27-22/h3-13H,2,14H2,1H3,(H,31,32)(H,26,27,28,29)

2-ethoxy-3-[[4-[2-(2H-tetrazol-5-yl)phenyl]phenyl]methyl]benzimidazole-4-carboxylic acid

CV11974; CV-11974, CV 11974, Trade names: Blopress, Atacand, Amias, and Ratacand

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)

Solubility in Formulation 1: ≥ 2.5 mg/mL (5.68 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 (5.68 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 3: 30%Propylene glycol, 5%Tween 80, 65% D5W:30 mg/mL

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