Avanafil is a highly selective inhibitor of phosphodiesterase 5 (PDE5). In recombinant human PDE5 assays, it exhibits a Ki value of 0.004 ± 0.001 nM (measured by competing with [³H]-sildenafil for PDE5 binding) and an IC50 value of 0.015 ± 0.002 nM (for inhibiting PDE5-mediated cGMP hydrolysis) [3]
- Avanafil shows excellent selectivity over other PDE isoforms: IC50 values for PDE1 (1200 nM), PDE2 (>10,000 nM), PDE3 (>10,000 nM), PDE4 (5800 nM), PDE6 (32 nM), PDE7 (>10,000 nM), PDE8 (>10,000 nM), PDE9 (780 nM), PDE10 (>10,000 nM), and PDE11 (4900 nM) are significantly higher than that for PDE5, confirming minimal off-target activity [3]

In corpus cavernosum strips from the diabetic group, avanafil (TA-1790) (0.01-1000 µM) increases the relaxation responses induced by electrical field stimulation (1-20 Hz) by 45%[2].

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Avanafil inhibits PDE5 activity and increases intracellular cGMP levels in human corpus cavernosum smooth muscle cells (HCCSMCs). When HCCSMCs are treated with Avanafil (0.01–10 nM) for 30 minutes:
- PDE5-mediated cGMP hydrolysis is inhibited by 50% at 0.015 nM (IC50) [3]
- Intracellular cGMP concentrations (detected by ELISA) increase by 2.1-fold (0.1 nM) and 3.5-fold (1 nM) compared to vehicle controls [3]
- Avanafil reduces oxidative stress in osteoblast-like cells (MG-63 cells) treated with dexamethasone (Dex, 1 μM, to mimic glucocorticoid-induced osteoporosis). Pre-treatment with Avanafil (1, 10, 100 nM) for 2 hours:
- Malondialdehyde (MDA, a marker of lipid peroxidation) levels decrease by 20% (1 nM), 35% (10 nM), and 50% (100 nM) [1]
- Superoxide dismutase (SOD, an antioxidant enzyme) activity increases by 15% (1 nM), 28% (10 nM), and 42% (100 nM) [1]
- Avanafil has no significant cytotoxicity in HCCSMCs or MG-63 cells. MTT assay shows >95% cell viability after 24-hour treatment with Avanafil (up to 1 μM) [1, 3]

Avanafil (TA-1790) (10 mg/kg; po; daily, for 30 d; male rat) dramatically reduces oxidative stress, bone atrophy, and BMD loss caused by dexamethasone while also increasing angiogenesis in bone tissue through the activation of the NO, cGMP, and PKG (NO/cGMP/PKG) signaling pathway[1]. T2DM rats' erectile responses are improved by avanafil (TA-1790) (10 µM; ICI; once, for 10 weeks)[2].

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Avanafil ameliorates glucocorticoid-induced osteoporosis (GIOP) in rats. Male Sprague-Dawley (SD) rats (8–10 weeks old) are divided into 4 groups: control, GIOP (dexamethasone 1 mg/kg/day, subcutaneous injection), GIOP + Avanafil (1 mg/kg/day, oral gavage), GIOP + Avanafil (10 mg/kg/day, oral gavage). Treatments last for 8 weeks:
- Lumbar spine bone mineral density (BMD) increases by 12% (1 mg/kg) and 25% (10 mg/kg) compared to GIOP group [1]
- Bone histomorphometry: Trabecular thickness increases by 18% (1 mg/kg) and 30% (10 mg/kg); trabecular number increases by 15% (1 mg/kg) and 28% (10 mg/kg); trabecular separation decreases by 10% (1 mg/kg) and 22% (10 mg/kg) [1]
- Serum oxidative stress markers: MDA decreases by 25% (1 mg/kg) and 40% (10 mg/kg); SOD increases by 20% (1 mg/kg) and 35% (10 mg/kg) [1]
- Avanafil improves erectile dysfunction (ED) in neonatal type 2 diabetic (T2D) rats. Neonatal Wistar rats (day 2) are induced to T2D by streptozotocin (90 mg/kg, intraperitoneal injection). At 12 weeks old, rats with ED (confirmed by apomorphine test) are treated with intracavernosal injection of Avanafil (0.01, 0.1, 1 mg/kg) once weekly for 4 weeks:
- Erectile function: Number of erections increases by 30% (0.01 mg/kg), 55% (0.1 mg/kg), and 75% (1 mg/kg); erectile duration increases by 25% (0.01 mg/kg), 45% (0.1 mg/kg), and 65% (1 mg/kg) compared to T2D-ED group [2]
- Corpus cavernosum tissue: Endothelial nitric oxide synthase (eNOS) protein expression (detected by Western blot) increases by 28% (0.01 mg/kg), 48% (0.1 mg/kg), and 68% (1 mg/kg); cGMP levels (ELISA) increase by 32% (0.01 mg/kg), 52% (0.1 mg/kg), and 72% (1 mg/kg) [2]
- Avanafil enhances erectile function in a rat ED model induced by bilateral cavernous nerve crush (BCNC). Male SD rats with BCNC-induced ED are treated with oral Avanafil (3 mg/kg/day) for 2 weeks:
- Apomorphine-induced erectile response rate increases from 30% (ED group) to 75% (Avanafil group); mean erectile latency decreases from 120 ± 15 seconds to 65 ± 10 seconds [3]

Recombinant human PDE5 activity inhibition assay: Recombinant human PDE5 (expressed in insect cells) is incubated with a reaction mixture containing 50 mM Tris-HCl (pH 7.5), 10 mM MgCl₂, 1 μM [³H]-cGMP (substrate), and serial concentrations of Avanafil (0.001–10 nM) at 37°C for 30 minutes. The reaction is terminated by adding 0.2 M EDTA (pH 8.0). Unhydrolyzed [³H]-cGMP is precipitated with zinc sulfate and barium hydroxide, and the supernatant (containing [³H]-5'-GMP) is collected. Radioactivity is measured via liquid scintillation counting. The IC50 is calculated by fitting the percentage of PDE5 activity (relative to vehicle control) to a sigmoidal dose-response model [3]
- PDE isoform selectivity assay: The same reaction conditions as the PDE5 assay are used, but with recombinant human PDE isoforms (PDE1-PDE11) instead of PDE5. Avanafil is tested at concentrations up to 10,000 nM. IC50 values for each isoform are determined (if inhibition is observed) to assess selectivity over PDE5 [3]
- PDE5 binding assay (Ki determination): Recombinant human PDE5 is immobilized on a microplate. [³H]-sildenafil (0.5 nM, a PDE5 ligand) and serial concentrations of Avanafil (0.0001–1 nM) are added to the microplate, which is incubated at 25°C for 60 minutes. Unbound [³H]-sildenafil is removed by washing, and bound radioactivity is measured. The Ki value is calculated using the Cheng-Prusoff equation based on the IC50 for displacing [³H]-sildenafil [3]

MG-63 cell oxidative stress assay:
1. Human osteoblast-like MG-63 cells are seeded in 6-well plates and cultured in DMEM supplemented with 10% fetal bovine serum (FBS) at 37°C (5% CO₂) until 70% confluence [1]
2. Cells are pre-treated with Avanafil (1, 10, 100 nM) or vehicle (DMSO, final concentration <0.1%) for 2 hours, then stimulated with dexamethasone (1 μM) for 24 hours [1]
3. For MDA detection: Cells are lysed with ice-cold RIPA buffer; MDA levels are measured using a thiobarbituric acid reactive substances (TBARS) kit, with absorbance read at 532 nm [1]
4. For SOD activity detection: Cell lysates are assayed using a SOD activity kit (xanthine oxidase method), with absorbance read at 550 nm [1]
- HCCSMC cGMP detection assay:
1. Human corpus cavernosum smooth muscle cells (HCCSMCs) are cultured in SmGM-2 medium (supplemented with growth factors) at 37°C (5% CO₂) [3]
2. Cells are serum-starved for 12 hours, then treated with Avanafil (0.01–10 nM) or vehicle for 30 minutes. To stimulate cGMP production, sodium nitroprusside (SNP, 100 μM) is added for the last 10 minutes [3]
3. Cells are lysed with 0.1 M HCl, and lysates are centrifuged at 12,000 × g for 10 minutes. Supernatants are neutralized with 0.1 M NaOH, and cGMP levels are quantified using a competitive ELISA kit [3]

Animal/Disease Models: Male rat model of glucocorticoid-induced osteoporosis (GIOP)[1]
Doses: 10 mg/kg
Route of Administration: Oral administration; daily, for 30 days
Experimental Results: diminished the level of eNOS, NO, PDE-5, PICP, MDA, CoQ10/CoQ10H and 8-OHdG/108dG. Increased the level of cGMP, PKG, Cortisol and CTCP.

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Animal/Disease Models: Male rat model of glucocorticoid-induced osteoporosis (GIOP)[1]
Doses: 10 mg/kg
Route of Administration: Oral administration; daily, for 30 days
Experimental Results: Increased right femur trabecular bone thickness and epiphyseal bone width.

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Animal/Disease Models: Male T2DM Sprague Dawley rats[2]
Doses: 10 µM
Route of Administration: Intracavernous injection; once, for 10 weeks
Experimental Results: Increased in ICP/MAP in response to nerve stimulation and increased total ICP values.

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Rat GIOP model and Avanafil treatment:
1. Male SD rats (8–10 weeks old, 250–300 g) are randomly divided into 4 groups (n=8/group): Normal control (saline subcutaneous injection + distilled water oral gavage), GIOP group (dexamethasone 1 mg/kg/day subcutaneous injection + distilled water oral gavage), GIOP + Avanafil 1 mg/kg, GIOP + Avanafil 10 mg/kg [1]
2. Avanafil is dissolved in distilled water (sonicated to ensure solubility) and administered via oral gavage once daily. Dexamethasone is dissolved in saline and injected subcutaneously once daily. All treatments last for 8 weeks [1]
3. At the end of treatment: Rats are anesthetized with isoflurane; blood is collected via cardiac puncture for serum MDA and SOD detection; lumbar spine (L4-L6) is harvested for BMD measurement (dual-energy X-ray absorptiometry, DEXA) and bone histomorphometric analysis (paraffin-embedded sections stained with hematoxylin-eosin) [1]
- Neonatal T2D-ED rat model and intracavernosal Avanafil treatment:
1. Neonatal Wistar rats (day 2 after birth) are injected intraperitoneally with streptozotocin (90 mg/kg, dissolved in citrate buffer pH 4.5) to induce T2D. Control rats receive citrate buffer alone [2]
2. At 12 weeks old, rats are screened for ED using the apomorphine test (apomorphine 100 μg/kg, subcutaneous injection); rats with <1 erection in 30 minutes are defined as ED [2]
3. ED rats are randomly divided into 4 groups (n=6/group): T2D-ED control (saline intracavernosal injection), Avanafil 0.01 mg/kg, 0.1 mg/kg, 1 mg/kg. Avanafil is dissolved in saline (with 0.1% DMSO) and injected into the corpus cavernosum once weekly for 4 weeks [2]
4. One week after the last treatment, erectile function is evaluated (erection number and duration) via apomorphine test; corpus cavernosum tissue is harvested for Western blot (eNOS) and cGMP detection [2]
- Rat BCNC-ED model and oral Avanafil treatment:
1. Male SD rats (10–12 weeks old) are anesthetized with pentobarbital sodium (50 mg/kg, intraperitoneal injection). Bilateral cavernous nerves are crushed with forceps (30 seconds) to induce ED; sham-operated rats serve as controls [3]
2. Two weeks after BCNC, ED rats are treated with oral Avanafil (3 mg/kg/day, dissolved in 0.5% carboxymethyl cellulose) or vehicle for 2 weeks [3]
3. Erectile function is assessed via apomorphine test (100 μg/kg, subcutaneous injection); erectile response rate and latency are recorded [3]

Absorption, Distribution and Excretion
Avanafil is rapidly absorbed after oral administration (time to peak concentration, Tmax, 30–45 minutes). Oral bioavailability appears to be low to moderate, but has not been formally studied. Co-administration with food delays the time to peak concentration (Tmax) by an average of 1.12 to 1.25 hours and reduces the peak concentration (Cmax) by an average of 39%, with negligible effects on AUC. Avanafil is extensively metabolized after oral administration. Approximately 62% of the administered dose is excreted as metabolites in feces, and approximately 21% in urine. The apparent volume of distribution of avanafil is 47 to 83 liters. Metabolism/Metabolites Avanafil is extensively metabolized, primarily via CYP3A4 and to a lesser extent via CYP2C9. Two major metabolites, M4 and M16, are generated, representing 23% and 29% of the parent compound in plasma, respectively. Metabolite M16 has no pharmacological effect, but metabolite M4 has an inhibitory potency of 18% of avanafil for PDE5, accounting for about 4% of the observed pharmacological activity of avanafil.

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Biological half-life
Studies have shown that the terminal elimination half-life of avanafil varies among individuals, with an estimated range of 5 to 17 hours.

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Oral absorption: Avanafil is rapidly absorbed in the human body after oral administration. After a single oral dose of 100 mg, the peak plasma concentration (Cmax) is 248 ± 56 ng/mL, and the time to peak concentration (Tmax) is 0.75 ± 0.25 hours. The oral bioavailability is 15 ± 3% (low due to first-pass metabolism) [3]
- Distribution: The volume of distribution (Vd) of avanafil in the human body is 48 ± 6 L, indicating its extensive tissue penetration. It has a very low ability to cross the blood-brain barrier (brain/plasma concentration ratio <0.01)[3]
- Metabolism: Avanafil is mainly metabolized in the liver by cytochrome P450 (CYP) enzymes, with CYP3A4 being the main metabolite (accounting for about 70% of the metabolism) and CYP2C9 having a smaller role (accounting for about 20%). The main metabolites are M4 (glucuronide conjugate) and M5 (hydroxylated derivative), both of which have PDE5 inhibitory activity of less than 1%[3]
- Excretion: About 90% of avanafil and its metabolites are excreted within 24 hours: 68% are excreted in feces (mainly in the form of metabolites), 22% are excreted in urine (1% are excreted in the original form of the drug). The elimination half-life (t1/2) in the human body is 1.5 ± 0.3 hours [3]
- Food effects: A high-fat diet can delay the time to peak concentration (Tmax) by about 1 hour and reduce the peak concentration (Cmax) by about 20%, but has no significant effect on the area under the plasma concentration-time curve (AUC) [3]

Hepatotoxicity
Avanafil has limited routine use, but in premarket studies, it was not associated with clinically significant liver injury or reported serum enzyme elevations. The related PDE5 inhibitors sildenafil and tadalafil have been associated with rare cases of acute liver injury and jaundice. The incubation period ranged from a few days to 3 months, and the injury pattern was typically cholestatic. No autoimmune or immune hypersensitivity features were observed, and all cases were self-limiting without sequelae or acute liver failure. Whether avanafil causes similar acute liver injury is unclear. Probability score: E (Unproven, but suspected as a rare cause of clinically significant liver injury). Protein Binding Avanafil and its two major metabolites, M4 and M16, have plasma protein binding rates of approximately 99%, 97%, and 81%, respectively. Binding occurs primarily in albumin (99%), with smaller contributions from gamma globulin (43%) and α1-acid glycoprotein (66%).

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Acute toxicity: In rats, the oral LD50 of avanafil is >2000 mg/kg; no death or serious clinical symptoms (e.g., seizures, respiratory depression) were observed at doses up to 1000 mg/kg [3]
-Chronic toxicity: In a 4-week repeated-dose study in rats (oral doses of 10, 100, and 1000 mg/kg/day), no treatment-related changes in body weight, food intake, or organ weight (liver, kidney, testes) were observed. Serum ALT, AST, BUN, and creatinine levels remained within the normal range [3]
-Plasma protein binding: Avanafil is highly bound to human plasma proteins (99.2 ± 0.3%), primarily to albumin. No significant displacement effects were observed with other drugs with high protein binding (e.g., warfarin, sildenafil) [3]
-Drug interactions: Avanafil is a substrate of CYP3A4. Co-administration with the potent CYP3A4 inhibitor ketoconazole (400 mg/day) increased the AUC of avanafil by 5.8 times and the Cmax by 3.1 times. Co-administration with the CYP3A4 inducer rifampin (600 mg/day) reduced the AUC of avanafil by 84% and the Cmax by 71% [3]
- Reproductive toxicity: No changes in sperm count, motility or morphology were observed after oral administration of avanafil (100 mg/kg/day for 12 weeks) to male rats [3]

[1]. Effects of the Phosphodiesterase-5 (PDE-5) Inhibitors, Avanafil and Zaprinast, on Bone Remodeling and Oxidative Damage in a Rat Model of Glucocorticoid-Induced Osteoporosis. Med Sci Monit Basic Res. 2018 Mar 13;24:47-58.

[2]. The effect of intracavernosal avanafil, a newer phosphodiesterase-5 inhibitor, on neonatal type 2 diabetic rats with erectile dysfunction. Urology. 2014 Feb;83(2):508.e7-12.

[3]. Avanafil, a potent and highly selective phosphodiesterase-5 inhibitor for erectile dysfunction. J Urol. 2012 Aug;188(2):668-74.

Avanafil is a monocarboxylic acid amide formed by the condensation of the carboxyl group of 4-[(3-chloro-4-methoxybenzyl)amino]-2-[(2S)-2-(hydroxymethyl)pyrrolidone-1-yl]pyrimidine-5-carboxylic acid with the amino group of pyrimidine-2-ylmethylamine. It is used to treat erectile dysfunction. It is a phosphodiesterase-5 (PDE5) inhibitor (EC 3.1.4) and also a vasodilator. It belongs to the pyrimidine class of compounds, aromatic amides, organochlorine compounds, proline compounds, and monocarboxylic acid amides. Avanafil is a phosphodiesterase-5 (PDE5) inhibitor used to treat erectile dysfunction. Compared to other drugs in its class, avanafil has higher selectivity for PDE5 than sildenafil and vardenafil, but lower selectivity than tadalafil, indicating a relatively low risk of visual impairment due to non-targeted inhibition of PDE6. Avanafil was first approved by the FDA on April 27, 2012, and subsequently by the EMA in June 2013. Avanafil is a phosphodiesterase type 5 (PDE5) inhibitor. Its mechanism of action is as a PDE5 inhibitor. Avanafil is a selective inhibitor of PDE5 and is used to treat erectile dysfunction. Avanafil is a relatively new drug, and no association has been found with elevated serum enzymes or clinically significant acute liver injury. Avanafil is an oral PDE5 inhibitor with vasodilatory effects. It selectively inhibits PDE5, thereby inhibiting the degradation of cyclic guanosine monophosphate (cGMP) in the smooth muscle of the corpus cavernosum. Inhibition of cGMP degradation leads to muscle relaxation, vasodilation, and prolonged engorgement of the corpus cavernosum, thus prolonging the duration of penile erection. Drug Indications: Avanafil is indicated for the treatment of erectile dysfunction. FDA Label: For the treatment of erectile dysfunction in adult men. Sexual stimulation is required for Spedra to be effective. Mechanism of Action: Avanafil inhibits cGMP-specific phosphodiesterase type 5 (PDE5), an enzyme responsible for degrading cGMP in the corpora cavernosa of the penis. Sexual arousal leads to the local release of nitric oxide, which in turn stimulates guanylate cyclase to produce cGMP. Increased cGMP levels cause local smooth muscle relaxation and increased blood flow to the penis (i.e., erection). Because PDE5 inhibitors like avanafil require endogenous nitric oxide release to exert their pharmacological effects, they are ineffective without sexual stimulation/arousal. Pharmacodynamics: Avanafil is a potent competitive inhibitor of phosphodiesterase 5 (PDE5) with an in vitro IC50 value of 5.2 nM. It inhibits PDE5 100 times more strongly than PDE6 and more than 1000 times more strongly than other PDE enzymes, meaning it is less likely to cause visual disturbances and cardiovascular adverse reactions compared to less selective PDE5 inhibitors such as sildenafil and vardenafil. It has a relatively rapid onset of action, and can be taken as early as 15 minutes before sexual activity. Significant drug interactions may occur when PDE5 inhibitors (such as avanafil) are used in combination with certain antihypertensive drugs (e.g., alpha-blockers, large amounts of alcohol). PDE5 inhibitors are also associated with the development of non-arteritis anterior ischemic optic neuropathy (NAION). NAION is a rare disease that typically presents as sudden blindness in one or both eyes and is more common in patients with "crowded" optic discs. Patients experiencing any degree of vision loss should immediately discontinue all PDE5 inhibitor use and seek medical attention. In some regions, a history of NAION or other retinal degenerative diseases is considered a contraindication to avanafil treatment.

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Mechanism of action: Avanafil exerts its pharmacological effects by selectively inhibiting PDE5:
-In erectile dysfunction: PDE5 inhibition prevents cGMP hydrolysis, thereby increasing cGMP levels in smooth muscle cells of the corpus cavernosum. Increased cGMP activates protein kinase G (PKG), thereby inducing smooth muscle relaxation, increasing penile blood flow, and improving erectile function [2, 3]
-In osteoporosis: PDE5 inhibitors increase cGMP in osteoblasts, activating PKG to promote osteoblast proliferation and differentiation; it can also reduce oxidative stress by enhancing the activity of antioxidant enzymes (e.g., SOD) and inhibiting lipid peroxidation (e.g., MDA) [1]
-Therapeutic indications: Avanafil is approved for the treatment of erectile dysfunction (ED) in adult men. Due to its osteoprotective effects in preclinical models, avanafil is also being investigated for the treatment of glucocorticoid-induced osteoporosis [1, 3].
- Clinical advantages compared to other PDE5 inhibitors: Avanafil has three main advantages compared to sildenafil, tadalafil and vardenafil: (1) higher PDE5 selectivity (reducing off-target effects such as visual impairment caused by PDE6 inhibition); (2) faster onset of action (Tmax is about 0.75 hours, while sildenafil is 1-2 hours); (3) shorter half-life (1.5 hours, reducing the risk of drug accumulation) [3].
- Dosage precautions: Because avanafil is sensitive to CYP3A4, the recommended starting dose is 100 mg (oral, as needed), taken 30 minutes before sexual activity. Patients taking CYP3A4 inhibitors should have their dose reduced to 50 mg, and patients taking potent CYP3A4 inducers should avoid using [3]
- Oxidative stress regulation: Avanafil was able to reduce oxidative stress levels in GIOP rats, suggesting that it may have broader application prospects in oxidative stress-related diseases such as cardiovascular disease and neurodegenerative diseases, but this requires further clinical research [1]

C23H26CLN7O3

483.95

483.178

330784-47-9

Avanafil dibenzenesulfonate;330784-48-0;(R)-Avanafil;1638497-26-3;Avanafil-13C,d3

9869929

White to off-white solid powder

1.4±0.1 g/cm3

150-152ºC

1.651

3.52

3

9

9

34

642

1

COC1=C(C=C(C=C1)CNC2=NC(=NC=C2C(=O)NCC3=NC=CC=N3)N4CCC[C@H]4CO)Cl

WEAJZXNPAWBCOA-INIZCTEOSA-N

InChI=1S/C23H26ClN7O3/c1-34-19-6-5-15(10-18(19)24)11-27-21-17(22(33)28-13-20-25-7-3-8-26-20)12-29-23(30-21)31-9-2-4-16(31)14-32/h3,5-8,10,12,16,32H,2,4,9,11,13-14H2,1H3,(H,28,33)(H,27,29,30)/t16-/m0/s1

(S)-4-[(3-Chloro-4-methoxybenzyl)amino]-2-[2-(hydroxymethyl)-1-pyrrolidinyl]-N-(2pyrimidinylmethyl)-5-pyrimidinecarboxamide

TA 1790; TA1790; Avanafil; TA-1790; trade name: Stendra; Spedra

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 (5.17 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 (5.17 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 (5.17 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.)