HIV-1
Suppression of insulin signaling pathway components: Insulin Receptor-β (IR-β), Insulin Receptor Substrate-1 (IRS-1), Phosphatidylinositol 3-kinase (PI3K/p85α), Akt (Protein Kinase B), and Endothelial Nitric Oxide Synthase (eNOS).

Nelfinavir (AG1341) Mesylate（1-10 μM；48 小时）可抑制多种骨髓瘤细胞的生长[4]。
Nelfinavir Mesylate 可抑制 26S 胰凝乳蛋白酶样蛋白酶体的活性，阻碍骨髓瘤细胞系增殖，并诱导细胞凋亡新生成的浆细胞[4]。
甲磺酸奈非那韦（1-10 μM；17 小时）细胞系在接触甲磺酸奈非那韦时会发生凋亡[4]。
甲磺酸奈非那韦（5 μM；0-24 小时）细胞凋亡减少AKT 磷酸化[4]。
甲磺酸奈非那韦导致 caspase-3 裂解，磷酸化 AKT、STAT-3 和 ERK1/2，并触发未折叠蛋白反应系统的促凋亡途径[4]。
Nelfinavir 的 IC50 为 35.93 μM，使其成为另一种 SARS-CoV 3CLpro 抑制剂[5]。

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用生理浓度（0.25 - 2 μg/mL）的 奈非那韦 慢性处理（72小时）人主动脉内皮细胞（HAECs），可显著降低基础性（2.5倍）和胰岛素诱导的（4至5倍）一氧化氮（NO）产生，该结果通过使用DAF-FM DA和DAF-2 DA染料的荧光测定法测得。
奈非那韦（1 和 2 μg/mL）以剂量依赖性的方式抑制了胰岛素诱导的Akt（Ser473位点）和eNOS（Ser1177位点）的磷酸化，该结果通过蛋白质免疫印迹法确定。
奈非那韦（1 和 2 μg/mL）抑制了胰岛素诱导的上游胰岛素信号组分IR-β、IRS-1和PI3K/p85α亚基的酪氨酸磷酸化，该结果通过免疫沉淀结合抗磷酸化酪氨酸抗体的免疫印迹法显示。
奈非那韦 对胰岛素诱导的Akt/eNOS磷酸化和NO产生的抑制作用，可通过与胰岛素增敏剂噻唑烷二酮类化合物曲格列酮（TRO, 250 nM）共处理而得到改善。
慢性 奈非那韦 暴露（2 μg/mL）也抑制了胰岛素诱导的eNOS基因（mRNA）表达，而TRO共处理可部分恢复此表达。[1]

Nelfinavir Mesylate（75 mg/kg；腹腔注射；每周 5 天，持续 21 天）抑制 NOD/SCID 小鼠中多发性骨髓瘤细胞的生长。

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在H157 NSCLC异种移植模型中，腹腔注射 奈非那韦 （50或100 mg/kg，每周5天）在第11天分别显著抑制肿瘤生长61%和63%。
在A549 NSCLC异种移植模型中，每日腹腔注射 奈非那韦 （50 mg/kg）在第19天抑制肿瘤生长48%。
口服灌胃给予 奈非那韦 （100 mg/kg，每周5天）也显著抑制了H157肿瘤生长。
来自 奈非那韦 治疗小鼠的肿瘤显示出凋亡增加（TUNEL阳性细胞）、ER扩张、自噬空泡存在（电镜），以及免疫印迹显示的磷酸化eIF2α、ATF3和LC3-II水平升高，证实了体内ER应激、自噬和凋亡的诱导。
肿瘤中的Akt磷酸化（S473）在体内未被 奈非那韦 处理所调节。

26S蛋白酶体活性实验： 裂解多发性骨髓瘤细胞。对于每个细胞系，将30 µg蛋白质收集在Tris缓冲液中，并与 奈非那韦、硼替佐米或MG132在37°C下孵育2小时。随后，加入1 mM荧光底物。使用Z-Leu-Leu-Val-Tyr-AMC底物测量糜蛋白酶样活性，使用Bz-Val-Gly-Arg-AMC底物测量胰蛋白酶样活性。使用荧光酶标仪测量酶活性。所有实验重复三次。

细胞培养与慢性药物处理： 原代人主动脉内皮细胞（HAECs）在内皮细胞生长培养基中培养。实验时，将融合度达70-80%的细胞用 奈非那韦（0.25, 0.5, 1, 2 μg/mL）和/或曲格列酮（TRO, 250 nM）处理总共72小时，每24小时更换含药培养基。慢性处理后，在分析前用胰岛素（100 ng/mL）刺激细胞10或15分钟。
一氧化氮（NO）测量 - 荧光显微镜法： 将培养在盖玻片上的HAECs，在药物处理和胰岛素刺激后，于黑暗中用荧光染料DAF-2 DA（5 μM）负载10分钟。然后洗涤、固定并封片。使用荧光显微镜（激发光480 nm，发射光505 nm）观察荧光（指示NO）。
一氧化氮（NO）测量 - 荧光测定法： 将培养在黑色96孔板中的HAECs，处理后用DAF-FM DA（5 μM）负载。孵育后，洗涤细胞并与L-精氨酸（100 μM）共孵育15分钟。使用荧光计（激发光485 nm，发射光525 nm）测量荧光值。数值均一化至总蛋白含量。
蛋白质免疫印迹分析： 处理后，裂解HAECs。蛋白质样品（≈50 μg）通过SDS-PAGE分离，转印至硝酸纤维素膜上，并用针对Akt（Ser473）、eNOS（Ser1177）、IR-β、IRS-1和PI3K/p85α的总蛋白及磷酸化形式的一抗进行孵育，随后使用HRP标记的二抗。通过化学发光法检测蛋白。
免疫沉淀： 为分析IR-β和IRS-1的酪氨酸磷酸化，将细胞裂解液（500 μg）与相应一抗孵育过夜。使用Protein A琼脂糖珠捕获免疫复合物，洗脱后，使用抗磷酸化酪氨酸抗体进行蛋白质免疫印迹分析。
逆转录聚合酶链反应（RT-PCR）： 使用TRIzol试剂从处理过的HAECs中提取总RNA。以1 μg RNA为模板合成cDNA。使用eNOS和GAPDH（内参基因）的特异性引物进行半定量PCR。PCR产物在琼脂糖凝胶上分离、染色，并对条带强度进行定量。[1]

NOD/SCID mice (bearing U266-luc cells)[4]
75 mg/kg
I.p.; 5 days a week for 21 days

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H157 Xenograft - Intraperitoneal Administration: Six-week-old male athymic nude mice were injected subcutaneously with H157 cells. When tumors were palpable, mice were divided into groups receiving i.p. injections of vehicle (4% DMSO, 5% polyethylene glycol, 5% Tween 80 in saline) or nelfinavir (50 or 100 mg/kg dissolved in vehicle) once daily on specified days (days 1-4, 7, 8, 10-12). Mice were weighed and tumors measured every other day.
A549 Xenograft - Intraperitoneal Administration: Six-week-old male athymic nude mice were injected subcutaneously with A549 cells in Matrigel. When tumors reached ~200 mm³, mice received daily i.p. injections of vehicle or nelfinavir (50 mg/kg). Mice were weighed and tumors measured three times weekly.
H157 Xenograft - Oral (Gavage) Administration: Eight-week-old female athymic nude mice bearing H157 xenografts received daily gavage (5 days/week) of vehicle or nelfinavir (100 mg/kg dissolved in 35% ethanol). Tumor volume was calculated using the formula (a b²) / 2.
Pharmacokinetic Study in Mice: Six-week-old female athymic nude mice received a single i.p. injection of nelfinavir (50 or 100 mg/kg in vehicle). Blood was collected via cardiac puncture at various time points under anesthesia. Plasma was separated and stored at -80°C until analysis by HPLC.
Tissue Analysis: Formalin-fixed, paraffin-embedded tumor sections were used for TUNEL staining according to kit instructions. For immunoblotting, frozen tumors were homogenized in lysis buffer.

Absorption, Distribution and Excretion
Distribution of nelfinavir into body tissues and fluids has not been fully characterized. The volume of distribution of nelfinavir following oral administration in animals is 27 L/kg, suggesting extensive tissue distribution. Studies in rats indicate that, at 4 hours after oral administration of radiolabeled nelfinavir, concentrations of the drug in liver, lymph nodes, pancreas, kidney, lungs, submaxillary glands, heart, and spleen exceed concurrent plasma concentrations. Nelfinavir has been detected in brain tissue in rats.
Nelfinavir is greater than 98% bound to plasma proteins, mostly to albumin and alpha1-acid glycoprotein. It is present in the CSF at less than 1% of plasma concentrations, at least in part due to its extensive binding to plasma protein but perhaps also due to the P-glycoprotein at the blood-brain barrier.
Nelfinavir and its metabolites are eliminated primarily in feces, with less than 2% of the drug being excreted in the urine. Moderate or severe liver disease may prolong the half-life and increase plasma concentrations of the parent drug while lowering plasma concentrations of M8 /(a major hydroxy-t-butylamide metabolite)/.
Nelfinavir absorption is very sensitive to food effects; a moderate fat meal increases the AUC 2 to 3 fold, and higher concentrations are achieved with high fat meals.
For more Absorption, Distribution and Excretion (Complete) data for NELFINAVIR MESYLATE (8 total), please visit the HSDB record page.

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Metabolism / Metabolites
Nelfinavir undergoes oxidative metabolism in the liver primarily by CYP3A4, but also by CYP2C19 and CYP2D6. Its major hydroxy-t-butylamide metabolite (M8) has in vitro antiretroviral activity comparable to that of the parent drug but achieves plasma levels that are only 40% of nelfinavir levels. The M8 metabolite is generated primarily by CYP2C19.

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Biological Half-Life
The plasma elimination half-life of nelfinavir in individuals 13 years of age and older is 3.5-5 hours.

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Following a single i.p. dose in mice, nelfinavir plasma concentrations peaked (Cmax) at 30 minutes: 23.21 μg/mL (~34.96 μmol/L) for 50 mg/kg and 54.33 μg/mL (~81.83 μmol/L) for 100 mg/kg.
The drug was rapidly cleared, with levels dropping to 0.1 μg/mL (~0.15 μmol/L) and 3 μg/mL (~4.5 μmol/L) for the 50 and 100 mg/kg groups, respectively, at 4 hours post-injection.
The area under the plasma concentration-time curve (AUC) was approximately 2.5-fold higher in the 100 mg/kg group (3445.53 minμg/mL) compared to the 50 mg/kg group (1398.26 minμg/mL).
The study mentions that the Cmax of nelfinavir in HIV patients is approximately 7-9 μmol/L, exceeding the mean in vitro GI50 of 5.2 μmol/L.
The human oral half-life is cited as 3-5 hours.

Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Nelfinavir levels in milk are low and the drug is usually not detectable in the serum of breastfed infants. However, some evidence of nelfinavir-induced adverse reactions in breastfed infants exists. Nelfinavir is not a recommended agent during breastfeeding. Achieving and maintaining viral suppression with antiretroviral therapy decreases breastfeeding transmission risk to less than 1%, but not zero. Individuals with HIV who are on antiretroviral therapy with a sustained undetectable viral load and who choose to breastfeed should be supported in this decision. If a viral load is not suppressed, banked pasteurized donor milk or formula is recommended.
◉ Effects in Breastfed Infants
A study compared the frequency of rash, hepatotoxicity, and hyperbilirubinemia among 464 breastfed infants whose mothers were taking either nelfinavir (n = 206) or nevirapine (n = 258) along with zidovudine and lamivudine for HIV infection during pregnancy and postpartum. Infants were examined during the first, second and sixth weeks postpartum. Moderate rash occurred in 7 (2.7%) of the infant exposed to nevirapine and one (0.5%) infant exposed to nelfinavir. Rash occurred at a median of 2 weeks postpartum. Four infants (1.9%) exposed to nelfinavir developed hepatotoxicity (3 moderate and 1 severe) and none exposed to nevirapine. Twenty-one infants (4.5%) developed high-risk hyperbilirubinemia, all prior to 48 hours of age, but there was no difference in exposure between the two drugs.
◉ Effects on Lactation and Breastmilk
Gynecomastia has been reported among men receiving highly active antiretroviral therapy. Gynecomastia is unilateral initially, but progresses to bilateral in about half of cases. No alterations in serum prolactin were noted and spontaneous resolution usually occurred within one year, even with continuation of the regimen. Some case reports and in vitro studies have suggested that protease inhibitors might cause hyperprolactinemia and galactorrhea in some male patients, although this has been disputed. The relevance of these findings to nursing mothers is not known. The prolactin level in a mother with established lactation may not affect her ability to breastfeed.

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Interactions
Exploiting protein homeostasis is a new therapeutic approach in cancer. Nelfinavir (NFV) is an HIV protease inhibitor that induces endoplasmic reticulum (ER) stress in cancer cells. Under conditions of ER stress, misfolded proteins are transported from the ER back to the cytosol for subsequent degradation by the ubiquitin-proteasome system. Bortezomib (BZ) is a proteasome inhibitor and interferes with degradation of misfolded proteins. Here, we show that NFV and BZ enhance proteotoxicity in non-small cell lung cancer (NSCLC) and multiple myeloma (MM) cells. The combination synergistically inhibited cell proliferation and induced cell death. Activating transcription factor (ATF)3 and CCAAT-enhancer binding protein homologous protein (CHOP), markers of ER stress, were rapidly increased, and their siRNA-mediated knockdown inhibited cell death. Knockdown of double-stranded RNA activated protein kinase-like ER kinase, a signal transducer in ER stress, significantly decreased apoptosis. Pretreatment with the protein synthesis inhibitor, cycloheximide, decreased levels of ubiquitinated proteins, ATF3, CHOP, and the overall total cell death, suggesting that inhibition of protein synthesis increases cell survival by relieving proteotoxic stress. The NFV/BZ combination inhibited the growth of NSCLC xenografts, which correlated with the induction of markers of ER stress and apoptosis. Collectively, these data show that NFV and BZ enhance proteotoxicity in NSCLC and MM cells, and suggest that this combination could tip the precarious balance of protein homeostasis in cancer cells for therapeutic gain.
Competition for the cytochrome p450 enzyme CYP3A by nelfinavir may inhibit the metabolism of these medications /amiodarone, astemizole, cisapride, ergot derivatives, midazolam, quinidine, terfenadine, triazolam/ and create the potential for serious and/or life threatening cardiac arrhythmias or prolonged sedation; concurrent use is not recommended.
Concurrent use /with lamivudine/ causes a 10% increase in the AUC of lamivudine.
Concurrent administration /of oral contraceptives such as: ethinyl estradiol or norethindrone/ with nelfinavir causes a decrease in the plasma concentrations of these medications; alternate or additional contraceptive measures should be used.
For more Interactions (Complete) data for NELFINAVIR MESYLATE (10 total), please visit the HSDB record page.

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The study states that Nelfinavir (a first-generation HIV protease inhibitor) is associated with severe metabolic side effects, including lipodystrophy, dyslipidemia, insulin resistance, and an increased risk of cardiovascular problems such as atherosclerosis and coronary artery disease in HIV patients on HAART.
The in vitro experiments used physiologically relevant concentrations of Nelfinavir (0.25-2 μg/mL), which are achievable in human plasma during therapy. [1]

[1]. Nelfinavir suppresses signaling and nitric oxide production by human aortic endothelial cells: protective effects of thiazolidinediones. Ochsner J. 2013 Spring;13(1):76-90.

[2]. Nelfinavir, A lead HIV protease inhibitor, is a broad-spectrum, anticancer agent that inducesendoplasmic reticulum stress, autophagy, and apoptosis in vitro and in vivo. Clin Cancer Res. 2007 Sep 1;13(17):5183-94.

[3]. Nelfinavir mesylate (AG1343): a potent, orally bioavailable inhibitor of HIV-1 protease. J Med Chem. 1997 Nov 21;40(24):3979-85.

[4]. The human immunodeficiency virus-1 protease inhibitor nelfinavir impairs proteasome activity and inhibits the proliferation of multiple myeloma cells in vitro and in vivo. Haematologica. 2012;97(7):1101‐1109.

[5]. Bardoxolone and bardoxolone methyl, two Nrf2 activators in clinical trials, inhibit SARS-CoV-2 replication and its 3C-like protease. Signal Transduct Target Ther. 2021 May 29;6(1):212.

Therapeutic Uses
HIV Protease Inhibitors.
HIV protease inhibitors are associated with HIV protease inhibitor-related lipodystrophy syndrome. Researchers hypothesized that liposarcomas would be similarly susceptible to the apoptotic effects of an HIV protease inhibitor, nelfinavir. We conducted a phase I trial of nelfinavir for liposarcomas. There was no limit to prior chemotherapy. The starting dose was 1,250 mg twice daily (Level 1). Doses were escalated in cohorts of three to a maximally evaluated dose of 4,250 mg (Level 5). One cycle was 28 days. Steady-state pharmacokinetics (PKs) for nelfinavir and its primary active metabolite, M8, were determined at Levels 4 (3,000 mg) and 5. Twenty subjects (13 males) were enrolled. Median (range) age was 64 years (37-81). One subject at Level 1 experienced reversible, grade 3 pancreatitis after 1 week and was replaced. No other dose-limiting toxicities were observed. Median (range) number of cycles was 3 (0.6-13.5). Overall best responses observed were 1 partial response, 1 minor response, 4 stable disease, and 13 progressive disease. Mean peak plasma levels and AUCs for nelfinavir were higher at Level 4 (7.3 mg/L; 60.9 mg/L X hr) than 5 (6.3 mg/L; 37.7 mg/L X hr). The mean ratio of M8: nelfinavir AUCs for both levels was approximately 1:3. PKs demonstrate auto-induction of nelfinavir clearance at the doses studied, although the mechanism remains unclear. Peak plasma concentrations were within range where anticancer activity was demonstrated in vitro. M8 metabolite is present at approximately 1/3 the level of nelfinavir and may also contribute to the anticancer activity observed.
Nelfinavir is indicated in the treatment of HIV infection when antiretroviral therapy is warranted. /Included in US product labeling/
A phase I/II dose-ranging open-label 28-day monotherapy study of the safety, pharmacokinetics, and antiviral activity of nelfinavir mesylate (Viracept), an inhibitor of human immunodeficiency virus (HIV)-1 protease, was done in 65 HIV-1-infected subjects. After 28 days, 54 responding subjects entered an open-label extension that allowed for the addition of nucleoside inhibitors of reverse transcriptase and dose escalation to maintain durability. The drug was well-tolerated and demonstrated robust antiviral activity, with demonstrable superiority of the 750 mg and 1000 mg three times daily regimens. Thirty subjects who continued to receive therapy at 12 months attained a persistent 1.6 log10 reduction in HIV RNA, accompanied by a mean increase in CD4 cells of 180-200/cu mm. Studies of viral genotype and phenotype after virus rebound revealed that the initial active site mutation allowing for nelfinavir resistance is mediated by a unique amino acid substitution in the HIV-1 protease D30N, which does not confer in vitro phenotypic cross-resistance to the currently available protease inhibitors.
For more Therapeutic Uses (Complete) data for NELFINAVIR MESYLATE (6 total), please visit the HSDB record page.

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Drug Warnings
In adults, the most frequent adverse effect associated with nelfinavir therapy is mild to moderate diarrhea.
Rash has been reported in 13% of adults receiving nelfinavir in the recommended dosage in phase II/III clinical studies. Allergic reaction, dermatitis, folliculitis, fungal dermatitis, maculopapular rash, pruritus, sweating, and urticaria have occurred in less than 2% of adults receiving nelfinavir in clinical studies. Hypersensitivity reactions, including bronchospasm, moderate to severe rash, fever, and edema, possibly related to nelfinavir have been reported during postmarketing surveillance.
In phase II/III clinical studies, asthenia occurred in 1% of adults receiving the usual dosage of nelfinavir in conjunction with 2 nucleoside reverse transcriptase inhibitors. Anxiety, depression, dizziness, emotional lability, headache (including migraine headache), hyperkinesia, insomnia,malaise, paresthesia, seizures, sleep disorders, somnolence, and suicidal ideation have been reported in less than 2% of adults receiving nelfinavir in clinical studies.
Substantial increases in serum concentrations of AST (SGOT) or ALT (SGPT) (increase from normal baseline values to 5.1-10 times the usual normal value or increase from baseline values of 1.25-2.5 times the normal value to more than 10 times the usual normal value) occurred in up to 3% of adults receiving nelfinavir in clinical studies. Hepatitis, increases in serum alkaline phosphate concentrations, increases in Gamma-glutamyltransferase (GGT, GGTP) concentrations, or abnormal liver function test results have been reported in less than 2% of adults receiving nelfinavir in clinical studies.
For more Drug Warnings (Complete) data for NELFINAVIR MESYLATE (19 total), please visit the HSDB record page.

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Nelfinavir is an HIV-1 protease inhibitor used in highly active antiretroviral therapy (HAART). This study investigates one of its major side effects: the induction of endothelial dysfunction.
The mechanism involves Nelfinavir suppressing the insulin-PI3K/Akt-eNOS signaling axis in endothelial cells, leading to reduced nitric oxide production, which is crucial for vascular homeostasis and vasodilation.
The study proposes that co-treatment with insulin-sensitizing thiazolidinediones (exemplified by Troglitazone) may protect against Nelfinavir-induced endothelial dysfunction, suggesting a potential adjunct therapy strategy. [1]

C33H49N3O7S2

663.8881

663.301

C, 59.70; H, 7.44; N, 6.33; O, 16.87; S, 9.66

159989-65-8

Nelfinavir;159989-64-7

64142

White to yellow solid powder

786.8ºC at 760 mmHg

131-135ºC

429.7ºC

6.052

189.95

5

9

10

45

922

5

S(C1C([H])=C([H])C([H])=C([H])C=1[H])C([H])([H])[C@@]([H])([C@@]([H])(C([H])([H])N1[C@]([H])(C(N([H])C(C([H])([H])[H])(C([H])([H])[H])C([H])([H])[H])=O)C([H])([H])[C@]2([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[C@]2([H])C1([H])[H])O[H])N([H])C(C1C([H])=C([H])C([H])=C(C=1C([H])([H])[H])O[H])=O.S(C([H])([H])[H])(=O)(=O)O[H]

NQHXCOAXSHGTIA-SKXNDZRYSA-N

InChI=1S/C32H45N3O4S.CH4O3S/c1-21-25(15-10-16-28(21)36)30(38)33-26(20-40-24-13-6-5-7-14-24)29(37)19-35-18-23-12-9-8-11-22(23)17-27(35)31(39)34-32(2,3)4;1-5(2,3)4/h5-7,10,13-16,22-23,26-27,29,36-37H,8-9,11-12,17-20H2,1-4H3,(H,33,38)(H,34,39);1H3,(H,2,3,4)/t22-,23+,26-,27-,29+;/m0./s1

(3S,4aS,8aS)-N-tert-butyl-2-[(2R,3R)-2-hydroxy-3-[(3-hydroxy-2-methylbenzoyl)amino]-4-phenylsulfanylbutyl]-3,4,4a,5,6,7,8,8a-octahydro-1H-isoquinoline-3-carboxamide;methanesulfonic acid

Nelfinavir mesylate hydrate; AG-1343; AG1343; AG 1343; Nelfinavir; Viracept

2934.99.9001

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（例如氮气保护），避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: ~100 mg/mL (~150.6 mM)
Ethanol: ~100 mg/mL (~150.6 mM)

配方 1 中的溶解度: ≥ 5 mg/mL (7.53 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。

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配方 2 中的溶解度: ≥ 5 mg/mL (7.53 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。

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配方 3 中的溶解度: ≥ 5 mg/mL (7.53 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 50.0 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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配方 4 中的溶解度: ≥ 2.5 mg/mL (3.77 mM) (饱和度未知) in 5% DMSO + 40% PEG300 + 5% Tween80 + 50% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
*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 5 中的溶解度: ≥ 2.5 mg/mL (3.77 mM) (饱和度未知) in 5% DMSO + 95% (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。
*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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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。