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]

在糖尿病组的海绵体条中，阿伐那非 (TA-1790) (0.01-1000 µM) 可使电场刺激 (1-20 Hz) 引起的松弛反应增加 45%[2]。

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阿伐那非（Avanafil） 抑制人海绵体平滑肌细胞（HCCSMCs）中的PDE5活性并升高细胞内cGMP水平。用0.01–10 nM的阿伐那非处理HCCSMCs 30分钟：
- PDE5介导的cGMP水解在0.015 nM（IC50）时被抑制50% [3]
- 细胞内cGMP浓度（ELISA检测）较溶剂对照组升高2.1倍（0.1 nM）和3.5倍（1 nM） [3]
- 阿伐那非（Avanafil） 降低地塞米松（Dex，1 μM，模拟糖皮质激素诱导骨质疏松）处理的成骨样细胞（MG-63细胞）氧化应激。用1、10、100 nM的阿伐那非预处理细胞2小时：
- 丙二醛（MDA，脂质过氧化标志物）水平分别降低20%（1 nM）、35%（10 nM）和50%（100 nM） [1]
- 超氧化物歧化酶（SOD，抗氧化酶）活性分别升高15%（1 nM）、28%（10 nM）和42%（100 nM） [1]
- 阿伐那非（Avanafil） 对HCCSMCs和MG-63细胞无显著细胞毒性。MTT实验显示，用阿伐那非（最高1 μM）处理24小时后，细胞存活率仍>95% [1, 3]

Avanafil (TA-1790)（10 mg/kg；口服；每日，持续 30 天；雄性大鼠）可显着减少地塞米松引起的氧化应激、骨萎缩和 BMD 损失，同时通过激活 NO 增加骨组织中的血管生成、cGMP 和 PKG (NO/cGMP/PKG) 信号通路[1]。阿伐那非 (TA-1790)（10 µM；ICI；一次，持续 10 周）可改善 T2DM 大鼠的勃起反应[2]。

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阿伐那非（Avanafil） 改善大鼠糖皮质激素诱导骨质疏松（GIOP）。8–10周龄雄性SD大鼠分为4组：对照组、GIOP组（地塞米松1 mg/kg/天，皮下注射）、GIOP+阿伐那非（1 mg/kg/天，灌胃）、GIOP+阿伐那非（10 mg/kg/天，灌胃），处理持续8周：
- 腰椎骨密度（BMD）较GIOP组分别升高12%（1 mg/kg）和25%（10 mg/kg） [1]
- 骨组织形态计量学：骨小梁厚度分别增加18%（1 mg/kg）和30%（10 mg/kg）；骨小梁数量分别增加15%（1 mg/kg）和28%（10 mg/kg）；骨小梁间距分别减少10%（1 mg/kg）和22%（10 mg/kg） [1]
- 血清氧化应激标志物：MDA分别降低25%（1 mg/kg）和40%（10 mg/kg）；SOD分别升高20%（1 mg/kg）和35%（10 mg/kg） [1]
- 阿伐那非（Avanafil） 改善新生2型糖尿病（T2D）大鼠勃起功能障碍（ED）。新生Wistar大鼠（出生后第2天）腹腔注射链脲佐菌素（90 mg/kg）诱导T2D，12周龄时通过阿扑吗啡实验筛选出ED大鼠，每周1次海绵体内注射阿伐那非（0.01、0.1、1 mg/kg），持续4周：
- 勃起功能：勃起次数较T2D-ED组分别增加30%（0.01 mg/kg）、55%（0.1 mg/kg）和75%（1 mg/kg）；勃起持续时间分别增加25%（0.01 mg/kg）、45%（0.1 mg/kg）和65%（1 mg/kg） [2]
- 海绵体组织：内皮型一氧化氮合酶（eNOS）蛋白表达（Western blot检测）分别增加28%（0.01 mg/kg）、48%（0.1 mg/kg）和68%（1 mg/kg）；cGMP水平（ELISA）分别增加32%（0.01 mg/kg）、52%（0.1 mg/kg）和72%（1 mg/kg） [2]
- 阿伐那非（Avanafil） 增强双侧海绵体神经压榨（BCNC）诱导ED大鼠的勃起功能。BCNC诱导ED的雄性SD大鼠口服阿伐那非（3 mg/kg/天）2周：
- 阿扑吗啡诱导勃起反应率从ED组的30%升至阿伐那非组的75%；平均勃起潜伏期从120±15秒降至65±10秒 [3]

人重组PDE5活性抑制实验：将人重组PDE5（昆虫细胞表达）与含50 mM Tris-HCl（pH 7.5）、10 mM MgCl₂、1 μM [³H]-cGMP（底物）及系列浓度阿伐那非（Avanafil）（0.001–10 nM）的反应体系在37°C孵育30分钟。加入0.2 M EDTA（pH 8.0）终止反应，用硫酸锌和氢氧化钡沉淀未水解的[³H]-cGMP，收集上清液（含[³H]-5'-GMP）。通过液体闪烁计数法检测放射性，将相对于溶剂对照组的PDE5活性百分比拟合至sigmoid剂量-反应模型，计算IC50 [3]
- PDE亚型选择性实验：采用与PDE5实验相同的反应条件，但用重组人PDE亚型（PDE1-PDE11）替代PDE5。阿伐那非的测试浓度高达10,000 nM，检测各亚型的IC50（若存在抑制）以评估对PDE5的选择性 [3]
- PDE5结合实验（Ki测定）：将人重组PDE5固定于微孔板，加入[³H]-西地那非（0.5 nM，PDE5配体）和系列浓度阿伐那非（0.0001–1 nM），25°C孵育60分钟。洗涤去除未结合的[³H]-西地那非，检测结合放射性。基于置换[³H]-西地那非的IC50，采用Cheng-Prusoff方程计算Ki值 [3]

MG-63细胞氧化应激实验：
1. 人成骨样MG-63细胞接种于6孔板，在含10%胎牛血清（FBS）的DMEM中37°C（5% CO₂）培养至70%融合 [1]
2. 细胞用阿伐那非（Avanafil）（1、10、100 nM）或溶剂（DMSO，终浓度<0.1%）预处理2小时，再用地塞米松（1 μM）刺激24小时 [1]
3. MDA检测：用冰浴RIPA缓冲液裂解细胞，采用硫代巴比妥酸反应底物（TBARS）试剂盒检测MDA水平，读取532 nm吸光度 [1]
4. SOD活性检测：采用SOD活性试剂盒（黄嘌呤氧化酶法）检测细胞裂解液SOD活性，读取550 nm吸光度 [1]
- HCCSMC细胞cGMP检测实验：
1. 人海绵体平滑肌细胞（HCCSMCs）在SmGM-2培养基（含生长因子）中37°C（5% CO₂）培养 [3]
2. 细胞饥饿12小时后，用阿伐那非（0.01–10 nM）或溶剂处理30分钟；最后10分钟加入硝普钠（SNP，100 μM）刺激cGMP生成 [3]
3. 用0.1 M HCl裂解细胞，裂解液12,000×g离心10分钟，上清液用0.1 M NaOH中和，采用竞争性ELISA试剂盒定量cGMP水平 [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 following oral administration (Tmax of 30-45 minutes) and appears to have low to moderate oral bioavailability, though formal studies have not been conducted. Administration with a meal results in a mean delay in Tmax of 1.12 to 1.25 hours, a 39% mean reduction in Cmax, and a negligible effect on AUC.
Following oral administration, avanafil is extensively metabolized. Approximately 62% of a given dose is excreted as metabolites in the feces and approximately 21% as metabolites in the urine.
The apparent volume of distribution of avanafil is 47 to 83 L.

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Metabolism / Metabolites
Avanafil is extensively metabolized, primarily by CYP3A4 and to a lesser extent by CYP2C9. There are two major metabolites formed, M4 and M16, which exist in the plasma at concentrations 23% and 29% that of the parent compound, respectively. The M16 metabolite lacks pharmacologic effect, but the M4 metabolite has an inhibitory potency for PDE5 18% that of avanafil and accounts for approximately 4% of the observed pharmacologic activity of avanafil.

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Biological Half-Life
Studies have demonstrated variability in the terminal elimination half-life of avanafil, with estimates ranging between 5 - 17 hours.

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Oral absorption: Avanafil is rapidly absorbed after oral administration in humans. A single oral dose of 100 mg achieves a peak plasma concentration (Cmax) of 248 ± 56 ng/mL at 0.75 ± 0.25 hours (Tmax). Oral bioavailability is 15 ± 3% (low due to first-pass metabolism) [3]
- Distribution: Avanafil has a volume of distribution (Vd) of 48 ± 6 L in humans, indicating extensive tissue penetration. It crosses the blood-brain barrier minimally (brain-to-plasma concentration ratio <0.01) [3]
- Metabolism: Avanafil is primarily metabolized in the liver by cytochrome P450 (CYP) enzymes, predominantly CYP3A4 (accounts for ~70% of metabolism) and to a lesser extent CYP2C9 (~20%). Major metabolites are M4 (glucuronide conjugate) and M5 (hydroxylated derivative), both with <1% of PDE5 inhibitory activity [3]
- Excretion: Approximately 90% of Avanafil and its metabolites are excreted within 24 hours: 68% in feces (mostly as metabolites) and 22% in urine (1% as unchanged drug). The elimination half-life (t1/2) is 1.5 ± 0.3 hours in humans [3]
- Food effect: A high-fat meal delays Tmax by ~1 hour and reduces Cmax by ~20%, but does not significantly affect the area under the plasma concentration-time curve (AUC) [3]

Hepatotoxicity
Avanafil has had limited general use, but in premarketing studies it was not associated with cases of clinically apparent liver injury and serum enzyme elevations were not reported. The related PDE5 inhibitors, sildenafil and tadalafil, have been linked to isolated, rare instances of acute liver injury and jaundice. The latency to onset ranged from a few days to 3 months and the pattern of injury was usually cholestatic. Autoimmune and immunoallergic features were not observed and all cases were self-limited without residual injury or acute liver failure. Whether avanafil can cause a similar form of acute liver injury is not yet known.
Likelihood score: E (unproved but suspected rare cause of clinically apparent liver injury).

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Protein Binding
Avanafil and its two major metabolites, M4 and M16, are highly protein-bound in plasma at approximately 99%, 97%, and 81%, respectively. Binding occurs primarily to albumin (99%), with smaller contributions from γ-globulin (43%) and α1-acid glycoprotein (66%).

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Acute toxicity: In rats, the oral median lethal dose (LD50) of Avanafil is >2000 mg/kg; no mortality or severe clinical signs (e.g., convulsions, respiratory depression) are 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, 1000 mg/kg/day), no treatment-related changes in body weight, food intake, or organ weights (liver, kidney, testis) are observed. Serum ALT, AST, BUN, and creatinine levels remain within normal ranges [3]
- Plasma protein binding: Avanafil has high plasma protein binding in humans (99.2 ± 0.3%), primarily binding to albumin. No significant displacement by other highly protein-bound drugs (e.g., warfarin, sildenafil) is observed [3]
- Drug-drug interactions: Avanafil is a substrate of CYP3A4. Co-administration with the strong CYP3A4 inhibitor ketoconazole (400 mg/day) increases Avanafil AUC by 5.8-fold and Cmax by 3.1-fold. Co-administration with the CYP3A4 inducer rifampicin (600 mg/day) decreases Avanafil AUC by 84% and Cmax by 71% [3]
- Reproductive toxicity: In male rats treated with oral Avanafil (100 mg/kg/day for 12 weeks), no changes in sperm count, motility, or morphology are observed [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 obtained by formal condensation of the carboxy group of 4-[(3-chloro-4-methoxybenzyl)amino]-2-[(2S)-2-(hydroxymethyl)pyrrolidin-1-yl]pyrimidine-5-carboxylic acid with the amino group of pyrimidin-2-ylmethylamine. Used for treatment of erectile dysfunction. It has a role as an EC 3.1.4. (phosphoric diester hydrolase) inhibitor and a vasodilator agent. It is a member of pyrimidines, an aromatic amide, an organochlorine compound, a member of prolinols and a monocarboxylic acid amide.
Avanafil is a phosphodiesterase-5 (PDE5) inhibitor used in the treatment of erectile dysfunction. In comparison with other drugs of the same class, it shows greater selectivity for PDE5 over PDE6 than both [sildenafil] and [vardenafil] but less selectivity than [tadalafil], suggesting a relatively lower risk of visual disturbances associated with off-target PDE6 inhibition. It first received FDA approval on April 27, 2012, with subsequent EMA approval in June 2013.
Avanafil is a Phosphodiesterase 5 Inhibitor. The mechanism of action of avanafil is as a Phosphodiesterase 5 Inhibitor.
Avanafil is a selective inhibitor of phosphodiesterase type 5 (PDE5) and is used as therapy of erectile dysfunction. Avanafil is a relatively new medication and has yet to be linked to instances of serum enzyme elevations or with clinically apparent acute liver injury.
Avanafil is an orally available phosphodiesterase type 5 (PDE5) inhibitor with vasodilatory activity. Avanafil selectively inhibits PDE5, thus inhibiting the degradation of cyclic guanosine monophosphate (cGMP) found in the smooth muscle of the corpus cavernosa of the penis. The inhibition of cGMP degradation results in prolonged muscle relaxation, vasodilation, and blood engorgement of the corpus cavernosa, thereby prolonging penile erection.

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Drug Indication
Avanafil is indicated for the treatment of erectile dysfunction.
FDA Label
Treatment of erectile dysfunction in adult men. In order for Spedra to be effective, sexual stimulation is required.

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Mechanism of Action
Avanafil inhibits the cGMP-specific phosphodiesterase type 5 (PDE5) which is responsible for the degradation of cGMP in the corpus cavernosum located around the penis. Sexual arousal results in the local release of nitric oxide, which in turn stimulates the enzyme guanylate cyclase to produce cGMP. Elevated levels of cGMP result in local smooth muscle relaxation and increased blood flow to the penis (i.e. an erection). As PDE5 inhibitors like avanafil require the endogenous release of nitric oxide in order to exert their pharmacologic effect, they have no effect on the user in the absence of sexual stimulation/arousal.

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Pharmacodynamics
Avanafil is a strong competitive inhibitor of phosphodiesterase 5 (PDE5) with a demonstrated _in vitro_ IC₅₀ of 5.2 nM. Its inhibitory effects on PDE5 are 100-fold more potent than on PDE6 and >1000-fold more potent than on other PDE enzymes, meaning it is less likely to cause visual disturbances and cardiovascular adverse effects when compared with less selective PDE5 inhibitors such as [sildenafil] and [vardenafil]. It has a relatively quick onset of action allowing for administration as early as 15 minutes prior to sexual activity. PDE5 inhibitors like avanafil can cause significant drug interactions when administered alongside certain antihypertensive agents (e.g. alpha blockers, substantial amounts of alcohol). PDE5 inhibitors have also been associated with the development of non-arteritic anterior ischemic optic neuropathy (NAION), a rare condition that typically presents as sudden loss of vision in one or both eyes and appears to be more common in patients with a \"crowded\" optic disc. Patients presenting with any degree of vision loss should immediately discontinue use of all PDE5 inhibitors and seek medical attention. In some jurisdictions, a history of NAION or other degenerative retinal disorders is considered a contraindication to avanafil therapy.

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Mechanism of action: Avanafil exerts its pharmacological effects by selectively inhibiting PDE5:
- In erectile dysfunction: PDE5 inhibition prevents cGMP hydrolysis, increasing intracellular cGMP levels in corpus cavernosum smooth muscle cells. Elevated cGMP activates protein kinase G (PKG), which induces smooth muscle relaxation, increases penile blood flow, and improves erectile function [2, 3]
- In osteoporosis: PDE5 inhibition increases cGMP in osteoblasts, activating PKG to promote osteoblast proliferation and differentiation; it also reduces oxidative stress by enhancing antioxidant enzyme (e.g., SOD) activity and suppressing lipid peroxidation (e.g., MDA) [1]
- Therapeutic indications: Avanafil is approved for the treatment of erectile dysfunction (ED) in adult males. It is also being investigated for potential use in glucocorticoid-induced osteoporosis due to its bone-protective effects in preclinical models [1, 3]
- Clinical advantages over other PDE5 inhibitors: Avanafil has three key advantages compared to sildenafil, tadalafil, and vardenafil: (1) Higher PDE5 selectivity (reducing off-target effects like visual disturbances from PDE6 inhibition); (2) Faster onset of action (Tmax ~0.75 hours, vs. 1–2 hours for sildenafil); (3) Shorter half-life (1.5 hours, reducing drug accumulation risk) [3]
- Dosage considerations: Due to its sensitivity to CYP3A4, the recommended starting dose of Avanafil is 100 mg (oral, as needed) 30 minutes before sexual activity. The dose is reduced to 50 mg in patients taking CYP3A4 inhibitors and avoided in patients taking strong CYP3A4 inducers [3]
- Oxidative stress regulation: Avanafil’s ability to reduce oxidative stress in GIOP rats suggests it may have broader applications in oxidative stress-related diseases, such as cardiovascular disease and neurodegenerative disorders, though this requires further clinical investigation [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

125.39

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)

配方 1 中的溶解度: ≥ 2.5 mg/mL (5.17 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (5.17 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (5.17 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。