| 规格 | 价格 | 库存 | 数量 |
|---|---|---|---|
| 10 mM * 1 mL in DMSO |
|
||
| 10mg |
|
||
| 50mg |
|
||
| 100mg |
|
||
| 250mg |
|
||
| 500mg |
|
||
| 1g |
|
||
| 2g |
|
||
| 5g |
|
||
| 10g |
|
||
| Other Sizes |
|
| 靶点 |
PDE5/phosphodiesterase 5
|
||
|---|---|---|---|
| 体外研究 (In Vitro) |
与单独5-羟色胺刺激相比，1 μM枸橼酸西地那非预处理可增强ERK1/ERK2磷酸化，增加S期细胞比例，促进细胞增殖（P<0.05）。用 1 μM 柠檬酸西地那非和血清素刺激预处理后，光密度（OD 值）突然上升至 0.33。这与单独的血清素刺激显着不同（P<0.05）。很明显，1 μM 西地那非会增加血清素诱导的 ERK1/ERK2 磷酸化的上调[2]。
|
||
| 体内研究 (In Vivo) |
柠檬酸西地那非可显着提高犬勃起模型中的 ICP 和 ICP/BP，但与媒介物相比对血压没有明显影响[1]。西地那非治疗在 10 mg/kg 时可显着减少 TL+ 细胞计数，但在 0.5 mg/kg 时则不会。在此阶段，用 PBS 处理的动物在缺血核心中具有 M1 样标记物 COX-2+ 呈阳性的细胞，而用 10 mg/kg 西地那非（但不是 0.5 mg/kg）处理的动物则大部分细胞处于缺血核心区。半影。相比之下，西地那非治疗（0.5 或 10 mg/kg 剂量）显着减少 pMCAo 后八天 Iba-1 染色的小胶质细胞/巨噬细胞的数量[3]。通过促进生长因子（FGF 和 VEGF）的释放，柠檬酸西地那非已被证明可以减少临床前动物模型中的皮瓣坏死。组织学也证明它对大鼠海绵体神经结构有效[4]。
|
||
| 酶活实验 |
所有关于ERK1/ERK2激活、MKP-1、PCNA表达以及细胞增殖和细胞周期分析的实验都是在第3-5代培养三天的细胞上进行的。此后，细胞在含有0.2%FBS和1%抗生素的RPMI-1640中血清饥饿三天。然后，细胞暴露于1μmol/L的血清素或西地那非，然后暴露于血清素，如图所示。在一些实验中，如所示，细胞在西地那非之前用10μmol/L的U0126预处理30分钟，随后暴露于血清素。在对照组中，用等体积的磷酸盐缓冲盐水（PBS）代替试剂。[2]
ERK1/ERK2磷酸化状态的免疫印迹分析[2] 如上所述，用血清素或1μmol/L的西地那非处理亚融合血清饥饿细胞，然后用或不用U0126刺激血清素。如上所述，在指定时间提取蛋白质。通过蛋白质印迹检测ERK1/ERK2蛋白的磷酸化。简而言之，通过SDS-PAGE分离等量的蛋白质（15-20μg），转移到聚偏二氟乙烯膜上，用抗磷酸化ERK1/ERK2抗体探测，并用辣根过氧化物酶（HRP）偶联的二抗检测。为了测定总ERK1/ERK2的表达，在50°C下用剥离缓冲液洗涤膜30分钟，然后用PBST中的5%牛血清白蛋白封闭膜4小时。此后，用特异性ERK1/ERK2抗体重新探测膜。 MKP-1、PCNA的免疫印迹分析[2] 如上所述，亚融合血清饥饿的PASMC在不同时间段内暴露于西地那非、血清素或U0126。在培养期结束时，提取蛋白质并用12%凝胶进行SDS-PAGE分离。然后将总蛋白转移到聚偏二氟乙烯膜上，在4°C下用PCNA和MKP-1抗体（1:1000）、甘油醛磷酸脱氢酶（GAPDH）抗体（1:2000）检测过夜。洗涤后，在室温下加入适当的二抗（1:5000）一小时。这些印迹是用Super Signal增强化学发光试剂盒开发的，并在柯达AR胶片上可视化。使用图像分析软件通过密度测定对条带进行定量。将蛋白质的相对表达标准化为GAPDH。 |
||
| 细胞实验 |
MTT比色法[2]
用0.1%胰蛋白酶/0.01%乙二胺四乙酸（EDTA）溶液收获约90%融合的细胞，以2x104个细胞/孔的密度接种到96孔板中，在含有10%FBS的RPMI-1640中生长三天，然后血清饥饿三天。然后将细胞与不同浓度的血清素或1μmol/L的 sildenafil/西地那非孵育不同时间，然后如所示，加入或不加入U0126的血清素。对照细胞以相同的方式处理，除了用无菌PBS代替药物。处理后，将培养基换成新鲜培养基，用5 g/L MTT孵育细胞4小时。然后用150μl 10%二甲亚砜（DMSO）溶解MTT 20分钟。使用微孔板读数器在570nm下测定96孔板中的光密度（OD）。 流式细胞术分析[2] 用0.1%胰蛋白酶/0.01%EDTA收获约90%融合的细胞，以5x104个细胞/孔的密度接种到6孔板中，在含有10%FBS的RPMI-1640中生长3天，然后血清饥饿3天。然后，如所示，将细胞与血清素或1μmol/L的 sildenafil/西地那非一起孵育24小时，然后用或不用U0126刺激血清素。用PBS冲洗细胞，用0.1%胰蛋白酶/0.01%EDTA溶液胰蛋白酶消化，并在20°C下以1000 r/min的速度离心5分钟收集细胞。将细胞颗粒在4°C的70%乙醇中固定至少24小时。用PBS洗涤固定的细胞两次，重新悬浮在含有50g/L RNase A和50mg/L碘化丙啶（PI）的PBS中。将悬浮液在37°C下孵育30分钟，通过200μm尼龙网过滤，然后通过流式细胞仪 进行分析。使用ModfitLT软件进行数据分析。S期细胞与所有G0G1+S+G2M期细胞的比率通过以下公式计算：S期分数（SPF）=S/（G0G1+S/G2M）x100% |
||
| 动物实验 |
|
||
| 药代性质 (ADME/PK) |
Absorption, Distribution and Excretion
Absorption Sildenafil is known to be quickly absorbed, with maximum plasma concentrations being observed within 30-120 minutes (with a median of 60 minutes) of oral administration in a fasting patient. Moreover, the mean absolute bioavailability observed for sildenafil is about 41% (from a range of 25-63%). In particular, after oral three times a day dosing of sildenafil, the AUC and Cmax increase in proportion with dose over the recommended dosage range of 25-100 mg. When used in pulmonary arterial hypertension patients, however, the oral bioavailability of sildenafil after a dosing regimen of 80 mg three times a day, was on average 43% greater than compared to the lower doses. Finally, if sildenafil is administered orally with food, the rate of absorption is observed to be decreased with a mean delay in Tmax of about 60 minutes and a mean decrease in Cmax of approximately 29%. Regardless, the extent of absorption is not observed to be significantly affected as the recorded AUC decreased by only about 11 %. Route of Elimination After either oral or intravenous administration, sildenafil is excreted as metabolites predominantly in the feces (approximately 80% of the administered oral dose) and to a lesser extent in the urine (approximately 13% of the administered oral dose). Volume of Distribution The mean steady-state volume of distribution documented for sildenafil is approximately 105 L - a value which suggests the medication undergoes distribution into the tissues. Clearance The total body clearance documented for sildenafil is 41 L/h. Sildenafil is rapidly and almost completely absorbed following oral administration. Bioequivalence has been established between the 20-mg tablet and the 10-mg/mL oral suspension when administered as a single oral dose of 20 mg. Although single-dose studies indicate that more than 90% of an oral sildenafil dose is absorbed from the GI tract, the drug undergoes extensive metabolism in the GI mucosa during absorption and on first pass through the liver, with only about 40% of a dose reaching systemic circulation unchanged. Pharmacokinetics of the drug (as determined by peak plasma concentrations or area under the plasma concentration-time curve (AUC)) are dose proportional over the single-dose range of 1.25-200 mg. Peak plasma concentrations of sildenafil and its active N-desmethyl metabolite are achieved within 30-120 (median: 60) minutes following oral administration in fasting adults. Sildenafil appears to be widely distributed in the body, with a reported volume of distribution at steady state averaging 105 L. It is not known whether sildenafil is distributed into milk. Sildenafil and its major circulating N-desmethyl metabolite are each approximately 96% bound to plasma proteins; protein binding reportedly is independent of plasma concentration over the range of 0.01-10 ug/mL. Plasma protein binding of the drug in geriatric adults older than 65 years of age is slightly greater (97%) than that observed in individuals younger than 45 years of age (96%). Sildenafil is distributed to a limited extent in semen following oral administration, with less than 0.001% of a single dose appearing in semen 90 minutes after dosing in healthy individuals Such concentrations are unlikely to cause any effects in sexual partners exposed to the semen. Sildenafil is eliminated mainly in the feces as metabolites. In healthy adults and those with erectile dysfunction, approximately 80% of an oral dose is excreted as metabolites in feces and 13% is excreted in urine. In volunteers with mild (CLcr=50-80 mL/min) and moderate (CLcr=30-49 mL/min) renal impairment, the pharmacokinetics of a single oral dose of Viagra (50 mg) were not altered. In volunteers with severe (CLcr=<30 mL/min) renal impairment, sildenafil clearance was reduced, resulting in approximately doubling of AUC and Cmax compared to age-matched volunteers with no renal impairment. View More
Metabolism / Metabolites
Biological Half-Life The terminal phase half-life observed for sildenafil is approximately 3 to 5 hours. Plasma sildenafil concentrations appear to decline in a biphasic manner following oral administration, with a terminal elimination half-life of about 4 hours (range: 3-5 hours). High clearance was the principal determinant of short elimination half-lives in rodents (0.4-1.3 hr), whereas moderate clearance in dog and man resulted in longer half-lives (6.1 and 3.7 hr respectively). |
||
| 毒性/毒理 (Toxicokinetics/TK) |
Toxicity Summary
IDENTIFICATION AND USE: Sildenafil is a white to off-white crystalline powder that is formulated into film-coated tablets, oral suspension, and parenteral injection. Sildenafil is a phosphodiesterase-5 (PDE-5) inhibitor. It is used both for the treatment of erectile dysfunction and for the treatment of pulmonary arterial hypertension (PAH) in adults to improve exercise ability and delay clinical worsening. HUMAN EXPOSURE AND TOXICITY: In general, overdosage of sildenafil may be expected to produce effects that are extensions of common adverse reactions. In studies of healthy individuals receiving single sildenafil doses up to 800 mg, the types of adverse events (e.g., decreased blood pressure, syncope, and prolonged erection) observed were similar to those observed at lower doses, but the incidences were increased. Serious adverse effects have also been reported at therapeutic dose levels including sudden decrease or loss of hearing, sudden loss of vision in one or both eyes, and prolonged erection lasting greater than 4 hours or priapism (a painful erection lasting greater than 6 hours). Serious cardiovascular, cerebrovascular, and vascular events, including myocardial infarction, sudden cardiac death, ventricular arrhythmia, cerebrovascular hemorrhage, transient ischemic attack, hypertension, subarachnoid and intracerebral hemorrhages, and pulmonary hemorrhage have been reported post-marketing in temporal association with the use of sildenafil for erectile dysfunction. Most, but not all, of these patients had preexisting cardiovascular risk factors. Therefore it was not possible to determine whether these events were related directly to sildenafil, to sexual activity, to the patient's underlying cardiovascular disease, to a combination of these factors, or to other factors. The use of sildenafil is not recommended in children. In a long-term trial in pediatric patients with PAH, an increase in mortality with increasing sildenafil dose was observed. Pulmonary vasodilators such as sildenafil may significantly worsen the cardiovascular status of patients with pulmonary veno-occlusive disease. Sildenafil profoundly potentiates the vasodilatory effects of organic nitrates and nitrites. The drug did not exhibit clastogenic potential in an in vitro human lymphocytes test system. ANIMAL STUDIES: Lethality after oral administration occurred at 1000 mg/kg and 500 mg/kg in rats and 1000 mg/kg in mice. Female rats were more affected than male rats. Acute sildenafil treatment stimulated testosterone production in adult male rats. There was no impairment of fertility in rats given sildenafil up to 60 mg/kg/day for 36 days to females and 102 days to males. However, in another study male rats were gavaged with sildenafil citrate (0.06 mg/0.05 mL) and allowed to mate. Fertilization rates and numbers of embryos were evaluated after treatment. Fertilization rates (day 1) were markedly reduced (approximately 33%) in matings where the male had taken sildenafil citrate. Over days 2-4, the numbers of embryos developing in the treated group were significantly fewer than in the control group. There was also a trend for impaired cleavage rates within those embryos, although this did not reach significance. No evidence of teratogenicity, embryotoxicity or fetotoxicity was observed in rats and rabbits which received up to 200 mg/kg/day during organogenesis. In another study, adult male rabbits received sildenafil at doses up to 9 mg/kg/day for 4 weeks to investigate the testicular histological alterations induced by overdoses of this drug. Abnormality in the germinal epithelium of the seminiferous tubules included spermatocytes karyopyknosis, spermatocytes degeneration, desquamation, spermatid giant cells and arrest of spermatogenesis. Additionally, increased Leydig cells cellularity, tubular degeneration, thickening of the interstitium were also observed. The encountered histological findings indicate that chronic exposure to sildenafil overdoses produces significant morphological and histological alterations in the testes which finally might lead to complete arrest of spermatogenesis. There was no evidence of carcinogenicity when sildenafil was administered orally to rats and mice for up to two years. Sildenafil did not exhibit evidence of mutagenicity in vitro in bacterial and Chinese hamster ovary cell assays. The drug also did not exhibit clastogenic potential in vivo in the mouse micronucleus test. Sildenafil is cleared predominantly by the CYP3A4 (major route) and CYP2C9 (minor route) hepatic microsomal isoenzymes. The major circulating metabolite results from N-desmethylation of sildenafil, and is itself further metabolized. This metabolite has a phosphodiesterase (PDE) selectivity profile similar to sildenafil and an in vitro potency for phosphodiesterase type 5 (PDE-5) approximately 50% of the parent drug. Plasma concentrations of this metabolite are approximately 40% of those seen for sildenafil, so that the metabolite accounts for about 20% of sildenafil's pharmacologic effects. Hepatotoxicity There have been at least 5 reports of acute liver injury attibuted to sildenafil use, but no instances of acute hepatic failure. The latency in most reports has been unclear because of the intermittent and sometimes unacknowledged use of sildenafil, but appears to be within 1 to 8 weeks. The pattern of serum enzyme elevations has ranged from hepatocellular to cholestatic, sometimes evolving from one to the other. The most convincing cases have been a mild cholestatic or "mixed" hepatitis arising within 1 to 3 months of starting sildenafil. Immunoallergic features and autoantibodies were not observed. Cases of acute onset with high serum aminotransferase levels have been reported after use of sildenafil that have some characteristics of ischemic injury. In other instances, the pattern of injury suggested anabolic steroid use. In two cases, re-exposure did not result in recurrence. Thus, the hepatotoxicity of sildenafil is not completely convincing and must be quite rare, if it occurs at all. Likelihood score: C (probable rare cause of clinically apparent liver injury). Effects During Pregnancy and Lactation View More
◉ Summary of Use during Lactation
Interactions Sildenafil and other phosphodiesterase (PDE) type 5 inhibitors (e.g., tadalafil, vardenafil) profoundly potentiate the vasodilatory effects (e.g., a systolic blood pressure reduction exceeding 25 mm Hg with sildenafil) of organic nitrates and nitrites (e.g., nitroglycerin, isosorbide dinitrate), and potentially life-threatening hypotension and/or hemodynamic compromise can result. Nitrates and nitrites promote the formation of cyclic guanosine monophosphate (cGMP) by stimulating guanylate cyclase, and PDE type 5 inhibitors (e.g., sildenafil, tadalafil, vardenafil) act to decrease the degradation of cGMP via phosphodiesterase (PDE) type 5 by inhibiting this enzyme, resulting in increased accumulation of cGMP and more pronounced smooth muscle relaxation and vasodilation than with either PDE type 5 inhibitors or nitrates/nitrites alone. This interaction probably occurs with any organic nitrate, nitrite, or nitric oxide donor (e.g., nitroprusside) regardless of their predominant hemodynamic site of action. Protein Binding It is generally observed that sildenafil and its main circulating N-desmethyl metabolite are both estimated to be about 96% bound to plasma proteins. Nevertheless, it has been determined that protein binding for sildenafil is independent of total drug concentrations. |
||
| 参考文献 |
|
||
| 其他信息 |
Sildenafil citrate is the citrate salt of sildenafil. It has a role as a vasodilator agent and an EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor. It contains a sildenafil.
Sildenafil Citrate is the citrate salt form of sildenafil, an orally bioavailable pyrazolopyrimidinone derivative structurally related to zaprinast, with vasodilating and potential anti-inflammatory activities. Upon oral administration, sildenafil selectively targets and inhibits cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5), thereby inhibiting the PDE5-mediated degradation of cGMP found in smooth muscle and increasing cGMP availability. This results in prolonged smooth muscle relaxation in the corpus cavernosum of the penis, thereby causing vasodilation, blood engorgement and a prolonged penile erection. In the smooth muscle of the pulmonary vasculature, the increase in cGMP results in smooth muscle relaxation, vasodilation of the pulmonary vascular bed, relieving pulmonary hypertension and increasing blood flow in the lungs. In addition, sildenafil may reduce airway inflammation and mucus production. A PHOSPHODIESTERASE TYPE-5 INHIBITOR; VASODILATOR AGENT and UROLOGICAL AGENT that is used in the treatment of ERECTILE DYSFUNCTION and PRIMARY PULMONARY HYPERTENSION. See also: Sildenafil (has active moiety). Drug Indication AdultsTreatment of adult patients with pulmonary arterial hypertension classified as WHO functional class II and III, to improve exercise capacity. Efficacy has been shown in primary pulmonary hypertension and pulmonary hypertension associated with connective tissue disease. Paediatric populationTreatment of paediatric patients aged 1 year to 17 years old with pulmonary arterial hypertension. Efficacy in terms of improvement of exercise capacity or pulmonary haemodynamics has been shown in primary pulmonary hypertension and pulmonary hypertension associated with congenital heart disease (see section 5. 1). AdultsTreatment of adult patients with pulmonary arterial hypertension classified as WHO functional class II and III, to improve exercise capacity. Efficacy has been shown in primary pulmonary hypertension and pulmonary hypertension associated with connective tissue disease. Paediatric populationTreatment of paediatric patients aged 1 year to 17 years old with pulmonary arterial hypertension. Efficacy in terms of improvement of exercise capacity or pulmonary haemodynamics has been shown in primary pulmonary hypertension and pulmonary hypertension associated with congenital heart disease. |
| 分子式 |
C22H30N6O4S.C6H8O7
|
|---|---|
| 分子量 |
666.7
|
| 精确质量 |
666.231
|
| 元素分析 |
C, 50.44; H, 5.75; N, 12.61; O, 26.40; S, 4.81
|
| CAS号 |
171599-83-0
|
| 相关CAS号 |
Sildenafil;139755-83-2;Sildenafil citrate-d8;1215071-03-6; 171599-83-0 (citrate); 252951-59-0 (nitrate)
|
| PubChem CID |
135413523
|
| 外观&性状 |
White to off-white solid powder
|
| 密度 |
1.447g/cm3
|
| 沸点 |
672.4ºC at 760 mmHg
|
| 熔点 |
187-189ºC
|
| 闪点 |
360.5ºC
|
| 蒸汽压 |
0mmHg at 25°C
|
| 折射率 |
1.683
|
| LogP |
1.319
|
| tPSA |
253.93
|
| 氢键供体(HBD)数目 |
5
|
| 氢键受体(HBA)数目 |
15
|
| 可旋转键数目(RBC) |
12
|
| 重原子数目 |
46
|
| 分子复杂度/Complexity |
1070
|
| 定义原子立体中心数目 |
0
|
| SMILES |
S(C1C([H])=C([H])C(=C(C2=NC3C(C([H])([H])C([H])([H])C([H])([H])[H])=NN(C([H])([H])[H])C=3C(N2[H])=O)C=1[H])OC([H])([H])C([H])([H])[H])(N1C([H])([H])C([H])([H])N(C([H])([H])[H])C([H])([H])C1([H])[H])(=O)=O.O([H])C(C(=O)O[H])(C([H])([H])C(=O)O[H])C([H])([H])C(=O)O[H]
|
| InChi Key |
DEIYFTQMQPDXOT-UHFFFAOYSA-N
|
| InChi Code |
InChI=1S/C22H30N6O4S.C6H8O7/c1-5-7-17-19-20(27(4)25-17)22(29)24-21(23-19)16-14-15(8-9-18(16)32-6-2)33(30,31)28-12-10-26(3)11-13-28;7-3(8)1-6(13,5(11)12)2-4(9)10/h8-9,14H,5-7,10-13H2,1-4H3,(H,23,24,29);13H,1-2H2,(H,7,8)(H,9,10)(H,11,12)
|
| 化学名 |
5-(2-ethoxy-5-((4-methylpiperazin-1-yl)sulfonyl)phenyl)-1-methyl-3-propyl-1,4-dihydro-7H-pyrazolo[4,3-d]pyrimidin-7-one 2-hydroxypropane-1,2,3-tricarboxylate
|
| 别名 |
UK-92480 citrate; UK 92480 citrate; Sildenafil Citrate; UK92480 citrate; UK 92480-10; 171599-83-0; Revatio; VIAGRA; Caverta; Sildenafil (citrate); Sildenafil citrate [USAN]; LIQREV; UK-92,480-10. Trade names: Revatio.
|
| HS Tariff Code |
2934.99.9001
|
| 存储方式 |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month 注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。 |
| 运输条件 |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| 溶解度 (体外实验) |
|
|||
|---|---|---|---|---|
| 溶解度 (体内实验) |
配方 1 中的溶解度: ≥ 5 mg/mL (7.50 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 50.0 mg/mL澄清DMSO储备液加入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。 配方 2 中的溶解度: ≥ 5 mg/mL (7.50 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 50.0 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。 View More
配方 3 中的溶解度: ≥ 5 mg/mL (7.50 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。 配方 4 中的溶解度: 30% PEG400+0.5% Tween80+5% propylene glycol:30 mg/mL 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。 |
| 制备储备液 | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.4999 mL | 7.4996 mL | 14.9993 mL | |
| 5 mM | 0.3000 mL | 1.4999 mL | 2.9999 mL | |
| 10 mM | 0.1500 mL | 0.7500 mL | 1.4999 mL |
1、根据实验需要选择合适的溶剂配制储备液 (母液)：对于大多数产品，InvivoChem推荐用DMSO配置母液 (比如：5、10、20mM或者10、20、50 mg/mL浓度），个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;
2、如果您找不到您想要的溶解度信息，或者很难将产品溶解在溶液中，请联系我们;
3、建议使用下列计算器进行相关计算（摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等）;
4、母液配好之后，将其分装到常规用量，并储存在-20°C或-80°C，尽量减少反复冻融循环。
计算结果:
工作液浓度： mg/mL；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL)。如该浓度超过该批次药物DMSO溶解度，请首先与我们联系。
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL ddH2O，混匀澄清。
(1) 请确保溶液澄清之后，再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶；
(2) 一定要按顺序加入溶剂 (助溶剂) 。
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT05558176 | Recruiting | Drug: Sildenafil citrate | Foetal Hypoxia | Ladoke Akintola University of Technology Teaching Hospital, Ogbomoso |
April 8, 2022 | Phase 4 |
| NCT02845388 | Completed | Drug: Sildenafil citrate Drug: estradiol valerate |
Infertility | Omar Ahmed El Sayed Saad | September 2015 | Phase 2 |
| NCT05951413 | Recruiting | Drug: Sildenafil Citrate Drug: estradiol |
IVF | Beni-Suef University | June 30, 2023 | Phase 2 Phase 3 |
| NCT03417492 | Terminated | Drug: Sildenafil Citrate | Traumatic Brain Injury Mild Traumatic Brain Injury |
University of Pennsylvania | March 1, 2018 | Phase 1 |
|
|---|
|
|
FCPR-16
Mardepodect盐酸盐
盐酸阿那格雷
己酮可可碱
InvivoChem的所有产品仅用于作科学研究，不面向患者销售
Copyright 2020 InvivoChem LLC | All Rights Reserved 粤ICP备20063088号-1
COA
粤公网安备 44011102003439号