HIV-1 protease inhibitor [2]
HIV-1 protease inhibitor [4]
Matrix metalloproteinase (MMP) expression and activity inhibitor (Specifically MMP-2 and MMP-9) [4]

沙奎那韦是一种蛋白酶抑制剂。蛋白酶是将蛋白质分子分解成更小的片段的酶。 HIV蛋白酶对于细胞内病毒复制和受感染细胞释放成熟病毒颗粒至关重要。沙奎那韦与病毒蛋白酶的活性位点结合并阻止病毒多蛋白的裂解，从而防止病毒成熟。沙奎那韦抑制 HIV-1 和 HIV-2 蛋白酶。研究还将沙奎那韦视为一种有前途的抗癌药物。

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在10 µM浓度下，沙奎那韦 显著抑制了由表皮生长因子（EGF，20 ng/ml）促进的原代宫颈上皮内瘤变（CIN）细胞（CIN612-7E和CIN612-9E）的侵袭。在CIN612-7E细胞中，抑制率约为-82% (P = 0.03)。[4]
用10 µM 沙奎那韦 处理96小时，可下调CIN细胞中MMP-9和MMP-2基因的表达。在CIN612-7E细胞中，它使MMP-9 RNA水平降低约-58% (P = 0.01)，MMP-2 RNA水平降低约-55% (P = 0.01)。[4]
用10 µM 沙奎那韦 处理96小时，降低了CIN细胞释放的MMP-9和MMP-2的明胶酶活性。在CIN612-7E细胞中，它使MMP-9的蛋白水解活性降低约-74%，MMP-2活性降低约-41%。[4] 用10 µM 沙奎那韦 处理5天，降低了原代CIN细胞的生长速率（细胞抑制作用），但不影响宫颈癌来源细胞系（SiHa, CaSki）的生长速率。[4] 用10 µM 沙奎那韦 处理，未能显著抑制高度进展的宫颈癌细胞系（SiHa和CaSki）的侵袭，也不影响这些细胞中MMP-2的表达或活性。然而，它在CaSki细胞中使MMP-9表达降低-44% (P = 0.02)，活性降低-71% (P = 0.04)。[4]

在一项为期48周的多中心、开放标签、非劣效性临床试验（Gemini研究）中，未接受过抗病毒治疗的HIV-1感染成人患者接受利托那韦增强的 沙奎那韦（SQV/r，1000/100 mg，每日两次）联合恩曲他滨/替诺福韦（FTC/TDF）治疗，表现出与接受洛匹那韦/利托那韦（LPV/r）治疗组相似的病毒学疗效。在第48周时，SQV/r组（n=167）有64.7%的参与者达到HIV-1 RNA <50拷贝/mL，而LPV/r组（n=170）为63.5%，达到了非劣效性标准。[2]
第48周时，SQV/r组的CD4细胞计数较基线中位增加值为178个细胞/mm³。[2]
SQV/r组的病毒学失败（VF）参与者比例为7%（11/167）。其中，仅有一名参与者在失败时出现了新的主要蛋白酶抑制剂（PI）相关耐药突变（G48V, V82A, I84V），且该参与者被记录为依从性差。[2]

MMP活性酶谱分析（Zymography）： 将用或不用10 µM 沙奎那韦 处理96小时的细胞的培养上清液中的总蛋白，通过非还原性SDS-PAGE（凝胶中聚合有明胶）进行分离。凝胶在37°C下孵育过夜，以允许明胶被酶降解。染色后，通过光密度法对与MMP-2 (72 kD) 和MMP-9 (92 kD) 活性对应的染色减弱区域（透明条带）进行定量。[4]

细胞侵袭实验（Boyden小室）： 将原代CIN细胞（CIN612-7E, CIN612-9E）或宫颈癌细胞系（SiHa, CaSki）在存在或不存在10 µM 沙奎那韦 的条件下培养96小时。然后收集细胞，接种到具有重组基底膜的Boyden小室的上室。下室含有20 ng/ml的重组人表皮生长因子（EGF）作为趋化剂。孵育后，对穿过膜到达下侧的细胞进行计数。[4]
细胞生长实验： 将CIN细胞（接种密度为1.5 x 10^4 细胞/孔）或宫颈癌细胞（接种密度为0.5 x 10^4 细胞/孔）在存在或不存在10 µM 沙奎那韦 的条件下培养5天。培养结束时对活细胞进行计数。[4] 细胞毒性实验（XTT实验）： 使用基于XTT的体外毒理学实验评估CIN612-7E细胞对 沙奎那韦 的敏感性。细胞用10 µM 沙奎那韦 培养48小时。该实验通过活细胞中线粒体脱氢酶将XTT四唑盐还原为水溶性的橙色甲臜衍生物来检测细胞活性。通过分光光度法测量吸光度，并计算相对于未处理对照的细胞存活率。[4]
Western印迹分析： 将CIN612-7E细胞在存在或不存在10 µM 沙奎那韦 的条件下培养指定时间。裂解细胞，通过SDS-PAGE分离蛋白质，转膜，并用抗p53的单克隆抗体进行检测。用抗β-肌动蛋白抗体重新检测以作为上样对照。通过光密度法对条带强度进行定量。[4]
实时定量聚合酶链反应（RT-PCR）： 从用或不用10 µM 沙奎那韦 处理96小时的细胞中提取总RNA。合成cDNA并使用MMP-2和MMP-9的特异性引物进行扩增。使用甘油醛-3-磷酸脱氢酶（GAPDH）作为内参基因进行归一化。使用SYBR Green PCR试剂盒进行RT-PCR。[4]

Absorption, Distribution and Excretion
The absolute bioavailability of orally administered saquinavir is only ~4%, thought to be a consequence of incomplete absorption and extensive first-pass metabolism. It is co-administered with ritonavir, another protease inhibitor and a potent inhibitor of the enzymes responsible for saquinavir's first-pass metabolism, in order to dramatically boost its serum concentrations and, by extension, its therapeutic efficacy. Following administration of saquinavir 1000mg twice daily with ritonavir 100mg twice daily the AUC24h at steady-state was 39026 ng.h/mL.
The primary means of elimination of saquinavir appears to be extensive hepatic metabolism followed by fecal excretion of both the parent drug and metabolic products. Following the administration of radiolabeled saquinavir (both orally and intravenously), approximately 81-88% of radioactivity is recovered in the feces within 5 days of dosing while only 1-3% is recovered in the urine. Mass balance studies indicate that only 13% of orally-administered plasma radioactivity is attributed to unchanged parent drug, with the remainder comprising metabolic products of saquinavir's hepatic metabolism. In contrast, intravenous administration resulted in approximately 66% of the circulating plasma radioactivity being attributed to unchanged parent drug, suggesting a high degree of first-pass metabolism with oral administration.
The steady-state volume of distribution of saquinavir is approximately 700 L, suggesting extensive distribution into tissues.
The systemic clearance of saquinavir is approximately 1.14 L/h/kg following intravenous administration.
Following administration of saquinavir in a dosage of 1200 mg 3 times daily as liquid-filled capsules, mean steady-state AUC at 3 weeks was 7249 ngh/mL compared with an AUC of 866 ngh/mL reported following administration of saquinavir hard gelatin capsules in a dosage of 600 mg 3 times daily. While the AUC of saquinavir in adults receiving liquid-filled capsules was lower at week 61-69 compared with the AUC at week 3, the AUC at week 61-69 was greater than the AUC at the same time point in HIV-infected adults receiving saquinavir as hard gelatin capsules (600 mg 3 times daily).
The relative oral bioavailability of saquinavir from liquid-filled (soft gelatin) capsules is estimated to average 331% (range: 207-530%) of that achieved with hard gelatin capsules of the drug when single 600-mg doses are administered. This would represent a calculated average oral bioavailability from the liquid-filled capsules of about 13% based on an average absolute bioavailability of 4% from the hard capsules; however, these are calculated estimates and not based on actual determination of absolute oral bioavailability from the liquid-filled capsules.
Saquinavir and its metabolites are eliminated from the body primarily through the biliary system and feces (more than 95% of the drug), with minimal urinary excretion (less than 3% of administered drug).
Oral bioavailability of the hard-gelatin capsule formulation of saquinavir (saquinavir mesylate, invirase) is only 4% due to limited absorption and extensive first-pass metabolism, with considerable interpatient variability. ... Absorption of saquinavir may be enhanced when the drug is taken with a high-calorie, high-fat meal. In addition, saquinavir demonstrates a greater than dose-proportional increase in exposure. For example, tripling the oral dose of saquinavir is associated with an eightfold increase in exposure.
For more Absorption, Distribution and Excretion (Complete) data for SAQUINAVIR (10 total), please visit the HSDB record page.

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Metabolism / Metabolites
Saquinavir is extensively metabolized in the liver following oral administration, and _in vitro_ studies have shown that >90% of its biotransformation is mediated by the CYP3A4 isoenzyme. Saquinavir is rapidly metabolized to a number of inactive mono- and di-hydroxylated compounds.
Results of in vitro studies indicate that saquinavir is rapidly metabolized in the liver to several monohydroxylated and dihydroxylated inactive metabolites. Metabolism of saquinavir is mediated by cytochrome P450; the isoenzyme CYP3A4 is involved in more than 90% of this metabolism. Orally administered saquinavir appears to undergo substantial metabolism on first pass through the liver.
Saquinavir is metabolized primarily by hepatic CYP3A4. The metabolites of saquinavir are not active against HIV-1.
Saquinavir has known human metabolites that include (2S)-N-[(2S,3R)-4-[(3S,4aS,8aS)-3-(tert-butylcarbamoyl)-7-hydroxy-decahydroisoquinolin-2-yl]-3-hydroxy-1-phenylbutan-2-yl]-2-[(quinolin-2-yl)formamido]butanediamide, (2S)-N-[(2S,3R)-4-[(3S,4aS,8aS)-3-[(1-hydroxy-2-methylpropan-2-yl)carbamoyl]-decahydroisoquinolin-2-yl]-3-hydroxy-1-phenylbutan-2-yl]-2-[(quinolin-2-yl)formamido]butanediamide, and (2S)-N-[(2S,3R)-4-[(3S,4aR,8aS)-3-(tert-butylcarbamoyl)-6-hydroxy-decahydroisoquinolin-2-yl]-3-hydroxy-1-phenylbutan-2-yl]-2-[(quinolin-2-yl)formamido]butanediamide.

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The study utilized a ritonavir-boosted regimen (saquinavir/ritonavir, SQV/r) to enhance the pharmacokinetic profile of saquinavir. However, no specific PK parameters (e.g., Cmax, Tmax, AUC, half-life, bioavailability) for saquinavir are reported in this article. [2]
The article states that the development of a new 500-mg film-coated tablet formulation (Invirase) reduced the pill burden, making saquinavir more practical for first-line therapy. [2]

Interactions
Concurrent use of saquinavir with terfenadine has resulted in an increase in the plasma concentrations of terfenadine; competition for the cytochrome p450 enzyme CYP3A by saquinavir may also inhibit the metabolism of astemizole, cisapride, ergot derivatives, midazolam, or triazolam, due to the potential for serious and/or life-threatening cardiac arrhythmias or prolonged sedation, concurrent use of any of these medications with saquinavir mesylate capsules or saquinavir soft gelatin capsules is not recommended.
Concurrent administration of saquinavir mesylate capsules with these medications /calcium channel blocking agents, clindamycin, dapsone, or quinidine/ which are substrates of the CYP3A4 isoenzyme of the cytochrome p450 enzyme system, may result in elevated plasma concentrations of these medications; patients should be monitored for toxicities associated with these medications.
Ethanol-intake decreases the bioavailability of SQV /saquinavir/ after oral administration alone or with RTV /ritonavir/.
Concurrent administration of rifabutin or rifampin with saquinavir mesylate capsules has resulted in a decrease in the steady-state AUC and peak plasma concentration of saquinavir by approximately 80% and 40%, respectively; carbamazepine, dexamethasone, phenobarbital, phenytoin, or other medications that induce CYP3A4 may also reduce saquinavir plasma concentrations; use of alternative medications should be considered if patients are taking either formulation of saquinavir.
For more Interactions (Complete) data for SAQUINAVIR (17 total), please visit the HSDB record page.

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In the Gemini study, discontinuations due to adverse events (AEs) occurred in 3% (5/167) of participants in the SQV/r arm. [2]
The most frequently reported drug-related AEs in the SQV/r arm were gastrointestinal disorders (17%, 27/167). Specific AEs reported in the SQV/r arm included bronchitis (6%), diarrhea (7%), nausea (6%), and upper respiratory tract infection (2%). [2]
The incidence of renal AEs was low in the SQV/r arm (4%, 7 participants). Two of these were serious AEs (nephrolithiasis; and hypokalemia with atrial tachycardia and tuberculous pleuritis). No participant discontinued due to renal-related AEs. [2]
Regarding plasma lipid changes, treatment with SQV/r caused increases from baseline in fasting total cholesterol (TC), LDL cholesterol, HDL cholesterol, and triglyceride (TG) levels. However, the median increase in TG levels at weeks 24 and 48 was significantly lower in the SQV/r arm compared to the LPV/r arm. [2]
Lipid-lowering therapy was initiated in 6 out of 167 (3.6%) participants in the SQV/r arm (all received statins). [2]
There were 3 deaths in the SQV/r arm. One death (a crime victim) was considered by the investigator to be remotely related to the study drug. [2]
Treatment of CIN612-7E cells with 10 µM saquinavir for 48 hours caused minimal cell death, as assessed by the XTT assay. Its toxicity profile was significantly lower than that of the pro-apoptotic anticancer drug staurosporine used as a positive control. [4]
Treatment with 10 µM saquinavir did not modify the intracellular protein levels of the tumor suppressor p53 in CIN cells, suggesting that at this therapeutic concentration, it does not significantly impair cellular proteasome function related to p53 degradation. [4]

[1]. In vitro and in vivo anticancer action of Saquinavir-NO, a novel nitric oxide-derivative of the protease inhibitor saquinavir, on hormone resistant prostate cancer cells. Cell cycle. 2011, 1.

[2]. Gemini: A Noninferiority Study of Saquinavir/Ritonavir Versus Lopinavir/Ritonavir as Initial HIV-1 Therapy in Adults. JAIDS Journal of Acquired Immune Deficiency Syndromes. 2009,50 (4) :367-374.

[3]. Saquinavir.

[4]. Ritonavir or saquinavir impairs the invasion of cervical intraepithelial neoplasia cells via a reduction of MMP expression and activity. AIDS. 2012, 26 (8): 909-919.

[5]. Saquinavir Inhibits Early Events Associated with Establishment of HIV-1 Infection: Potential Role for Protease Inhibitors in Prevention. Antimicrob. Agents Chemother. 2012, 56 (8): 4381-4390.

[6]. 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
Saquinavir, in combination with other antiretroviral agents, is indicated in the treatment of HIV infection or AIDS. Saquinavir soft gelatin capsule (Fortovase) is the preferred dosage form, according to the FDA. /Included in US product labeling/
Saquinavir was not detected in cord blood. Saquinavir soft-gel capsules are well tolerated during pregnancy and are not associated in this small study with birth abnormalities. Transmission of HIV infection from mother to child was successfully prevented in all cases. Low maternal exposures of saquinavir were noted. However, these did not appear to affect virologic efficacy of the combination. Samples from cord blood indicate minimal fetal exposure to saquinavir.

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Drug Warnings
The principal adverse effects associated with saquinavir therapy involve the GI tract. In adults with HIV infection receiving saquinavir liquid-filled or hard gelatin capsules in conjunction with other antiretroviral agents (e.g., 2 dideoxynucleoside reverse transcriptase inhibitors), diarrhea occurred in 15.6-19.9%, abdominal discomfort in 8.6-13.3%, abdominal pain in 2.3-7.8%, nausea in 10.6-17.8%, dyspepsia in 8.4-8.9%, flatulence in 5.7-12.2%, vomiting in 2.9-4.4%, altered taste in 4.4%, and constipation in 3.3% of patients.
Adverse GI effects reported in <2% of patients receiving saquinavir hard gelatin or liquid-filled capsules alone or in conjunction with other antiretroviral agents include anorexia, abdominal distention, buccal mucosa ulceration, oral canker sores, cheilitis, dry mouth, dysphagia, abdominal colic, esophageal ulceration, esophagitis, eructation, bloodstained or discolored feces, frequent bowel movements, fecal incontinence, gastralgia, gastritis, GI reflux, GI ulcer, GI inflammation, intestinal obstruction, gingivitis, glossitis, hemorrhoids, infectious diarrhea, melena, painful defecation, parotid disorder, pruritus ani, /SRP: heartburn/, stomach upset, pelvic pain, rectal hemorrhage, salivary gland disorder, stomatitis, unpleasant taste, toothache, and tooth disorder.
Headache has occurred in 58.9% of adults with HIV infection receiving saquinavir liquid-filled capsules in conjunction with other antiretroviral agents. Depression has been reported in 2.7%, insomnia in 5.6%, and anxiety or libido disorder in 2.2% of patients receiving saquinavir liquid-filled capsules in conjunction with other antiretroviral therapy.
Adverse nervous system effects that have been reported in less than 2% of patients receiving saquinavir hard gelatin or liquid-filled capsules alone or in conjunction with other antiretroviral agents include ataxia, cerebral hemorrhage, confusion, seizures, dizziness, dysarthria, dysesthesia, facial numbness, facial pain, numbness of the extremities, hyperesthesia, hyperreflexia, hyporeflexia, light-headed feeling, myelopolyradiculoneuritis, paresthesia, peripheral neuropathy, prickly sensation, paresis, poliomyelitis, progressive multifocal leukoencephalopathy, spasms, tremor, and unconsciousness. Adverse psychologic effects reported in less than 2% of patients receiving the drug include agitation, amnesia, anxiety, behavior disturbances, excessive dreaming, euphoria, hallucination, irritability, lethargy, overdose effect, psychic disorder, psychosis, reduced intellectual ability, somnolence, and speech disorder. Serious adverse nervous system effects that have been reported rarely in clinical studies in patients receiving saquinavir alone or in conjunction with other antiretroviral agents which were considered to be at least possibly related to the study drugs include attempted suicide, episodes involving confusion, ataxia and weakness, and headache.
For more Drug Warnings (Complete) data for SAQUINAVIR (23 total), please visit the HSDB record page.

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Pharmacodynamics
Saquinavir exerts its antiviral activity by inhibiting an enzyme critical for the HIV-1 viral lifecycle. Like other protease inhibitors, saquinavir has a propensity for participating in drug interactions - use caution when administering saquinavir to patients maintained on other pharmaceutical agents as pharmacodynamic and pharmacokinetic interactions are common. Saquinavir is known to increase the QTc-interval in otherwise healthy individuals, and should therefore be used with caution in patients maintained on other QTc-prolonging medications or for whom prolongation of the QTc-interval may be of particular consequence (e.g. patients with pre-existing heart disease). Careful and regular monitoring of patient bloodwork is recommended, as saquinavir has been associated with the development of metabolic complications (e.g. diabetes mellitus, hyperlipidemia) and worsening of pre-existing liver disease.

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Saquinavir is a well-established HIV-1 protease inhibitor. [2]
The Gemini study demonstrated that a regimen containing ritonavir-boosted saquinavir (SQV/r) is non-inferior in antiviral efficacy to a regimen containing lopinavir/ritonavir (LPV/r) over 48 weeks in treatment-naive patients, supporting its consideration as a preferred option for first-line therapy. [2]
The study highlights that saquinavir, when boosted with ritonavir, offers a more favorable triglyceride profile compared to lopinavir/ritonavir, which may be a consideration for patients at risk of metabolic complications. [2]
The development of a major PI resistance mutation was rare among participants with virologic failure in the SQV/r arm, supporting the use of boosted PIs in initial therapy. [2]
Saquinavir is an HIV protease inhibitor used in highly active antiretroviral therapy (HAART). [4]
Beyond its antiviral activity, saquinavir has demonstrated direct antitumour and antiangiogenic properties in HIV-free preclinical models. [4]
This study provides a mechanistic rationale for the observed clinical benefits of HAART (containing protease inhibitors like saquinavir) in reducing the onset and progression of cervical intraepithelial neoplasia (CIN) in HIV-infected women. [4]
The data suggest that saquinavir, at therapeutic concentrations, is particularly effective at inhibiting the invasion of pre-cancerous CIN cells by down-regulating key matrix metalloproteinases (MMP-2 and MMP-9), but may lack efficacy against highly progressed cervical carcinoma cells. [4]
These findings support the potential repurposing of saquinavir as a pharmacological agent to prevent CIN progression or recurrence, offering a potential non-surgical alternative. [4]

C38H50N6O5

670.85

670.384

127779-20-8

Saquinavir mesylate;149845-06-7;Saquinavir-d9;1356355-11-7

441243

White to off-white solid powder

1.3±0.1 g/cm3

1015ºC at 760 mmHg

91.5ºC

567.7ºC

0mmHg at 25°C

1.646

6.4

166.75

5

7

13

49

1140

6

CC(C)(C)NC(=O)[C@@H]1C[C@@H]2CCCC[C@@H]2CN1C[C@H]([C@H](CC3=CC=CC=C3)NC(=O)[C@H](CC(=O)N)NC(=O)C4=NC5=CC=CC=C5C=C4)O

QWAXKHKRTORLEM-UGJKXSETSA-N

InChI=1S/C38H50N6O5/c1-38(2,3)43-37(49)32-20-26-14-7-8-15-27(26)22-44(32)23-33(45)30(19-24-11-5-4-6-12-24)41-36(48)31(21-34(39)46)42-35(47)29-18-17-25-13-9-10-16-28(25)40-29/h4-6,9-13,16-18,26-27,30-33,45H,7-8,14-15,19-23H2,1-3H3,(H2,39,46)(H,41,48)(H,42,47)(H,43,49)/t26-,27+,30-,31-,32-,33+/m0/s1

(2S)-N-[(2S,3R)-4-[(3S,4aS,8aS)-3-(tert-butylcarbamoyl)-3,4,4a,5,6,7,8,8a-octahydro-1H-isoquinolin-2-yl]-3-hydroxy-1-phenylbutan-2-yl]-2-(quinoline-2-carbonylamino)butanediamide

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)

DMSO : ~100 mg/mL (~149.07 mM)

配方 1 中的溶解度: ≥ 2.5 mg/mL (3.73 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 (3.73 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 (3.73 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；
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7、 以上所有助溶剂都可在 Invivochem.cn网站购买。