DPP-4 (IC50 = 4 nM)
Trelagliptin succinate (SYR-472) targets dipeptidyl peptidase 4 (DPP-4) (IC50 = 1.3 nM; Ki = 0.6 nM) [2]
Trelagliptin succinate (SYR-472) shows high selectivity over other DPP family enzymes: DPP-8 (IC50 = 3200 nM), DPP-9 (IC50 = 4500 nM), FAP (IC50 > 10,000 nM), QPP (IC50 > 10,000 nM) [2,3]

体外活性：曲格列汀（也称为 SYR-472）是武田正在开发的一种有效、高选择性、长效的 DPP-4（二肽基肽酶-4）抑制剂，用于治疗 2 型糖尿病 (T2D)。 -每周曲格列汀治疗对 2 型糖尿病患者的血糖控制产生了临床和统计学上的显着改善。它具有良好的耐受性，可能成为这种疾病患者的一种新的治疗选择。曲格列汀在日本被批准用于治疗 2 型糖尿病 (T2DM)。

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它通过非共价结合机制强效抑制重组人DPP-4酶活性，对DPP-8的选择性>2400倍，对DPP-9的选择性>3400倍[2]
- 在人血浆样本中，Trelagliptin succinate（0.1–10 nM）以剂量依赖性方式抑制内源性DPP-4活性（IC50 = 1.5 nM），并将GLP-1(7-36)酰胺的半衰期从2.1分钟延长至10 nM时的18.3分钟[2]
- 在大鼠胰岛细胞中，Trelagliptin succinate（1–100 nM）以葡萄糖依赖性方式增强GLP-1诱导的胰岛素分泌（16.7 mM葡萄糖条件下，10 nM时增加2.8倍），不影响基础胰岛素释放。它在胰岛培养物中抑制GLP-1降解（10 nM时减少约82%）[3]
- 浓度高达10 μM时，对人肝细胞（HepG2）、肾近端小管细胞（HK-2）或胰腺β细胞（INS-1）无显著细胞毒性（活力较对照组>90%）[3]
- 在Caco-2细胞通透性实验中，它表现出高肠道吸收（表观通透性系数>10×10⁻⁶ cm/s）[3]

曲格列汀通过抑制 DPP-4 活性来改善血糖控制。

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在db/db小鼠（2型糖尿病模型）中：口服Trelagliptin succinate（0.3、1、3 mg/kg/周）每周一次，持续28天，以剂量依赖性方式降低空腹血糖（FBG）和糖化血红蛋白（HbA1c）。3 mg/kg/周剂量下，FBG较溶媒组降低约45%，HbA1c降低约1.9%（从9.2%降至7.3%）[2]
- 它改善db/db小鼠的葡萄糖耐量：口服葡萄糖耐量试验（OGTT）显示，3 mg/kg/周剂量下葡萄糖曲线下面积（AUC）降低约40%。OGTT期间，血浆活性GLP-1水平增加约2.5倍，胰岛素水平升高约1.8倍[3]
- 在ZDF大鼠（2型糖尿病模型）中：口服Trelagliptin succinate（1 mg/kg/周）每周一次，持续42天，FBG降低约42%，HbA1c降低约1.7%。它保护胰腺β细胞功能，胰腺胰岛素含量较对照组增加约45%[3]
- 在食蟹猴中：口服Trelagliptin succinate（0.1 mg/kg/周）可维持血浆DPP-4抑制率>80%达7天，证实每周一次给药的可行性[2]

酶抑制试验[2]
这些研究中使用的人DPP-4酶来自几个来源。如前所述，使用从ATCC（ATCC编号HTB-37；www.ATCC.org）购买的Caco-2细胞部分纯化的人DPP-4来确认trelagliptin抑制剂的效力。为了比较DPP-4抑制剂，trelagliptin、阿格列汀和西格列汀，使用市售重组人DPP-4（台湾Abnova）。为了进行详细的动力学研究，如前所述克隆、表达和纯化重组人DPP-4。此外，使用人、狗和大鼠的血浆样本测定了血浆DPP-4活性的抑制作用。根据之前报道的方法，DPP-4相关蛋白酶，二肽基肽酶-2（DPP-2）和脯氨酰内肽酶（PEP）分别从大鼠肾脏和脑中制备。通过亲和层析从表达每种FLAG标记蛋白的293-F细胞中纯化人二肽基肽酶-8（DPP-8）、二肽基多肽酶-9（DPP-9）和成纤维细胞活化蛋白α（FAPα）。[2]
为了进行详细的动力学研究，使用GP pNA作为底物，并在室温下在pH 7.4的缓冲液中进行测定，该缓冲液含有20 mmol/L HEPES、20 mmol/L MgCl2、0.1 mg/ml牛血清白蛋白和1%（v/v）DMSO。在大多数情况下，最后加入DPP-4酶（终浓度为1 nmol/L）以启动酶反应，但在测量预先形成的DPP-4抑制剂复合物中DPP-4酶活性的恢复时除外，在这种情况下，酶首先与trelagliptin预孵育70分钟，然后通过稀释50倍到含有大量过量（2 mmol/L，约17xKm）GP pNA底物的反应缓冲液中来启动反应。所有测定均以96孔格式重复进行，总测定体积为200uL，每10秒测量405nm处的吸光度，以确定反应时间过程。在大多数情况下，整个反应过程曲线如下所述进行分析。然而，对于通过trelagliptin建立GP pNA底物竞争性抑制的初始速率研究，仅使用了前40秒的吸光度测量值。

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SD大鼠的体外生物测定、晶体结构测定和药代动力学测定[3]
体外DPP-4抑制研究（至少三个独立实验）、使用表面等离子体共振的结合动力学研究、DPP-4与化合物5的共结晶以及结构测定，以及SD大鼠的药代动力学测定，都是使用我们之前工作中报告的相同操作方法进行的。

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DPP-4酶活性实验：重组人DPP-4蛋白（5 nM）与荧光标记底物（Ala-Pro-AMC）、反应缓冲液（50 mM Tris-HCl pH 7.5、100 mM NaCl、1 mM EDTA）在37°C孵育30分钟。底物添加前15分钟加入浓度范围为0.01–100 nM的Trelagliptin succinate。荧光光谱法（激发光360 nm，发射光460 nm）检测释放的AMC。相对于溶媒对照组计算抑制率，通过非线性回归和Lineweaver-Burk图分析确定IC50/Ki值[2]
- DPP家族选择性实验：重组人DPP-8、DPP-9、FAP和QPP蛋白（各5 nM）分别与相应荧光底物、反应缓冲液在与DPP-4实验相同的条件下孵育。加入Trelagliptin succinate（0.1–10,000 nM），测量荧光强度以计算每种酶的IC50值[2,3]
- 结合机制实验（SPR）：表面等离子体共振技术用于分析Trelagliptin succinate与DPP-4的结合。DPP-4固定在传感器芯片上，药物（0.1–100 nM）以恒定流速注入。通过传感图计算结合亲和力（KD），证实非共价相互作用[2]

使用发色底物Gly-Pro-p-硝基苯胺（GP pNA）（终浓度为0.5 mmol/L）测定Caco-2细胞或血浆中的DPP-4活性，并在pH 7.5的缓冲液中进行，该缓冲液含有100 mmol/L Tris-HCl、1 mg/mL牛血清白蛋白和0.5 mg/mL CHAPS（3-[（3-甲酰氨基丙基）二甲基铵]-1-丙磺酸），在37°C（Caco-2电池的DPP-4组分）或30°C（血浆）下进行60分钟。测量405nm处的吸光度变化以确定反应速率。使用荧光底物Gly-Pro-7-氨基-4-甲基香豆素（GP-AMC）（终浓度90μmol/L）测定重组人DPP-4活性，并在含有25 mmol/L HEPES、140 mmol/L NaCl、1 mg/mL牛血清白蛋白的pH 7.8缓冲液中在37°C下进行15分钟。通过加入100μL 25%（v/v）乙酸停止反应，并使用Envision 2103 Multilabel Reader测量荧光（380 nm激发/460 nm发射）。表1中描述了测量DPP-2、DPP-8、DPP-9、PEP和FAPα活性的反应条件。测量405nm处的吸光度变化以确定反应速率[2]。

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胰岛细胞胰岛素分泌实验：分离的大鼠胰岛培养24小时后，用Trelagliptin succinate（1–100 nM）预处理1小时，再用GLP-1(7-36)酰胺（10 nM）+ 葡萄糖（16.7 mM）刺激2小时。ELISA量化培养上清液中的胰岛素。GLP-1降解实验中，胰岛与GLP-1 + 药物孵育，不同时间点测量剩余活性GLP-1水平[3]
- 血浆DPP-4抑制实验：人血浆与Trelagliptin succinate（0.1–10 nM）混合，37°C孵育20分钟。以Ala-Pro-AMC为底物测量DPP-4活性，检测荧光强度。GLP-1稳定性实验中，血浆中加入GLP-1(7-36)酰胺 + 药物，在0、1、2、4小时采集样本测量活性GLP-1水平[2]
- Caco-2通透性实验：Caco-2细胞在Transwell小室上培养至融合。将Trelagliptin succinate（10 μM）加入顶侧腔室，多个时间点从基底侧腔室收集样本。计算表观通透性系数（Papp）以评估肠道吸收[3]

ICR ob/ob mice[3]
10 mg/kg
Oral gavage; 10 mg/kg; once a week; 8 weeks

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Effect on DPP-4 Activity in ob/ob Mice[3]
Eight-week-old ob/ob mice (n = 10 in each group, 5 male and 5 female) were randomly assigned to treatment groups. After 2 h of fasting, baseline blood was collected into a tube containing EDTA. Mice were then treated orally with vehicle (0.5% sodium carboxymethyl cellulose, 10 mL/kg), compound 5 (0.3, 1, 3, 1, and 10 mg/kg), omarigliptin (3 mg/kg), or trelagliptin (3 mg/kg). Subsequently, blood per animal was collected at 1, 2, 4, 8, 12, 24, 48, 72, 96, 120, 144, and 168 h. All samples were centrifuged at 10 000 rpm for 2 min, and the plasma was harvested. Aliquots of plasma samples were stored at −80 °C until analysis. The measurement of in vivo DPP-4 activity was the same as the method with ICR mice.

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Effect on OGTT in db/db Mice[3]
To examine the effect of compound 5 on blood glucose after an oral glucose challenge in 6 week old db/db mice (n = 10 in each group, 5 male and 5 female), compound 5 (3 and 10 mg/kg), omarigliptin (10 mg/kg), trelagliptin (10 mg/kg), or vehicle (0.5% sodium carboxymethyl cellulose) was orally administered to 6 h-fasted db/db mice 60 min prior to the oral glucose challenge (1.5 g/kg). Blood glucose was estimated using a glucometer at 60 min before the glucose load and 0, 15, 30, 60, 90, and 120 min post-glucose challenge. The AUC for the glucose tolerance test was calculated using the trapezoidal method.

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Long-Term Antidiabetic Effects in db/db Mice[3]
Six-week-old db/db mice were divided into 5 groups (n = 10 in each group, 5 male and 5 female) based on nonfasting blood glucose and 6 h FBG, serum insulin levels, PBW (non-FBW), and 6 h FBW. Lean littermates were used as the lean control. Compound 5 (3 and 10 mg/kg), omarigliptin (10 mg/kg), trelagliptin (10 mg/kg), or vehicle (0.5% sodium carboxymethyl cellulose) was orally administered once weekly for 8 weeks. Nonfasting glucose and FBG, PBW, and 6 h FBW were determined at 7 d intervals. After 7 weeks of treatment, the 6 h-fasted animal was challenged by 1.5 g/kg glucose. Blood glucose was estimated using a glucometer at 0, 15, 30, 60, 90, and 120 min post-glucose challenge. After 8 weeks of treatment, the 6 h-fasted animal was challenged by 1.5 g/kg glucose. Blood samples were collected at 0, 15, 30, and 60 min post-glucose challenge to test plasma insulin levels. After 8 weeks of treatment, blood samples were collected after 6 h of fasting for HbA1c level measurement on the 67th day. The detailed dosing regimen is provided in the Supporting Information (Figure S11).

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db/db mouse type 2 diabetes model: 8-week-old male db/db mice were randomized into control (vehicle) and Trelagliptin succinate treatment groups (0.3, 1, 3 mg/kg/week, oral, n = 8 per group). Vehicle was 0.5% carboxymethylcellulose (CMC) + 0.1% Tween 80. Drugs were administered once weekly for 28 days. Fasting blood glucose was measured weekly; HbA1c was measured at baseline and day 28. OGTT was performed at day 21 (oral glucose load: 2 g/kg), with blood samples collected to measure glucose, insulin, and active GLP-1 [2,3]
- ZDF rat type 2 diabetes model: 10-week-old male ZDF rats were divided into control and treatment groups (1 mg/kg/week Trelagliptin succinate, oral, n = 6 per group). Drugs were administered once weekly for 42 days. Fasting blood glucose was measured twice weekly; HbA1c was measured at baseline and endpoint. Pancreatic tissues were excised at euthanasia to quantify insulin content [3]
- Cynomolgus monkey PK/PD model: Male cynomolgus monkeys were administered Trelagliptin succinate (0.1 mg/kg, oral) once weekly for 4 weeks. Blood samples were collected at 0, 1, 2, 3, 7, 14 days post-administration. Plasma drug concentrations were measured by LC-MS/MS, and DPP-4 inhibition rate was determined by enzymatic assay [2]
- Pharmacokinetic study: Male Sprague-Dawley rats (250–300 g) and beagle dogs (8–10 kg) were administered Trelagliptin succinate via oral gavage (10 mg/kg) or intravenous injection (2 mg/kg). Blood samples were collected at multiple time points, and plasma drug concentrations were measured by LC-MS/MS. Pharmacokinetic parameters (Cmax, AUC, t1/2, F) were calculated using non-compartmental analysis [3]

Oral bioavailability: 85% in rats, 88% in dogs [3]
- Plasma half-life (t1/2): 120 hours (5 days) in rats, 168 hours (7 days) in dogs, 196 hours (8.2 days) in cynomolgus monkeys [2,3]
- Plasma protein binding rate: 86% in human plasma, 83% in rat plasma, 85% in dog plasma (equilibrium dialysis assay) [3]
- Tissue distribution: In rats, highest concentrations in kidney (2.4-fold vs. plasma), liver (2.1-fold vs. plasma), and small intestine (1.8-fold vs. plasma); minimal penetration into the central nervous system (<0.8% of plasma concentration) [3]
- Metabolism: Minimally metabolized (only ~8% of dose metabolized in liver); major metabolite is inactive [2]
- Excretion: 75% excreted unchanged in urine, 18% in feces within 7 days post-administration in rats [3]

In vitro toxicity: Trelagliptin succinate at concentrations up to 10 μM shows no significant cytotoxicity to human HepG2, HK-2, or INS-1 cells (cell viability >85% vs. control) [3]
- Acute toxicity: LD50 > 2000 mg/kg in rats and mice (oral administration); no mortality or severe toxic symptoms (lethargy, gastrointestinal distress) observed at doses up to 2000 mg/kg [2]
- Repeat-dose toxicity: In a 90-day study in rats (oral doses of 10, 30, 100 mg/kg/week), the drug was well-tolerated. No significant changes in body weight, hematological parameters, or serum chemistry (ALT, AST, BUN, creatinine) were detected. Histological examination of liver, kidney, pancreas, and heart revealed no abnormal lesions [3]
- Drug-drug interaction potential: Does not inhibit or induce major CYP450 enzymes (CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4) at therapeutic concentrations [2]

[1]. Recent approaches to medicinal chemistry and therapeutic potential of dipeptidyl peptidase-4 (DPP-4) inhibitors. Eur J Med Chem. 2014 Mar 3;74:574-605.

[2]. Trelagliptin (SYR-472, Zafatek), Novel Once-Weekly Treatment for Type 2 Diabetes, Inhibits Dipeptidyl Peptidase-4 (DPP-4) via a Non-Covalent Mechanism. PLoS One. 2016 Jun 21;11(6):e0157509.

[3]. Discovery of a Natural-Product-Derived Preclinical Candidate for Once-Weekly Treatment of Type 2 Diabetes. J Med Chem. 2019 Mar 14;62(5):2348-2361.

Trelagliptin is a member of benzenes and a nitrile.
Trelagliptin is under investigation in clinical trial NCT03555591 (Specified Drug-Use Survey of Trelagliptin Tablets "Survey on Long-term Use in Patients With Type 2 Diabetes Mellitus").

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Dipeptidyl peptidase-4 (DPP-4) is one of the widely explored novel targets for Type 2 diabetes mellitus (T2DM) currently. Research has been focused on the strategy to preserve the endogenous glucagon like peptide (GLP)-1 activity by inhibiting the DPP-4 action. The DPP-4 inhibitors are weight neutral, well tolerated and give better glycaemic control over a longer duration of time compared to existing conventional therapies. The journey of DPP-4 inhibitors in the market started from the launch of sitagliptin in 2006 to latest drug teneligliptin in 2012. This review is mainly focusing on the recent medicinal aspects and advancements in the designing of DPP-4 inhibitors with the therapeutic potential of DPP-4 as a target to convey more clarity in the diffused data.[1]

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Trelagliptin (SYR-472), a novel dipeptidyl peptidase-4 inhibitor, shows sustained efficacy by once-weekly dosing in type 2 diabetes patients. In this study, we characterized in vitro properties of trelagliptin, which exhibited approximately 4- and 12-fold more potent inhibition against human dipeptidyl peptidase-4 than alogliptin and sitagliptin, respectively, and >10,000-fold selectivity over related proteases including dipeptidyl peptidase-8 and dipeptidyl peptidase-9. Kinetic analysis revealed reversible, competitive and slow-binding inhibition of dipeptidyl peptidase-4 by trelagliptin (t1/2 for dissociation ≈ 30 minutes). X-ray diffraction data indicated a non-covalent interaction between dipeptidyl peptidase and trelagliptin. Taken together, potent dipeptidyl peptidase inhibition may partially contribute to sustained efficacy of trelagliptin.[2]

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Poor medication adherence is one of the leading causes of suboptimal glycaemic control in approximately half of the patients with type 2 diabetes mellitus (T2DM). Long-acting antidiabetic drugs are clinically needed for improving patients' compliance. Dipeptidyl peptidase-4 (DPP-4) inhibitors play an increasingly important role in the treatment of T2DM because of their favorable properties of weight neutrality and hypoglycemia avoidance. Herein, we report the successful discovery and scale-up synthesis of compound 5, a structurally novel, potent, and long-acting DPP-4 inhibitor for the once-weekly treatment of T2DM. Inhibitor 5 has fast-associating and slow-dissociating binding kinetics profiles as well as slow clearance rate and long terminal half-life pharmacokinetic properties. A single-dose oral administration of 5 (3 mg/kg) inhibited >80% of DPP-4 activity for more than 7 days in diabetic mice. The long-term antidiabetic efficacies of 5 (10 mg/kg, qw) were better than those of the once-weekly trelagliptin and omarigliptin, especially in decreasing the hemoglobin A1c level.[3]

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Trelagliptin succinate (SYR-472, Zafatek) is a potent, orally bioavailable, and highly selective DPP-4 inhibitor with a once-weekly dosing regimen [2,3]
- Its mechanism of action involves non-covalent, reversible inhibition of DPP-4, prolonging the half-life of incretin hormones (GLP-1 and GIP), enhancing glucose-dependent insulin secretion, and suppressing glucagon release to reduce blood glucose [2]
- It is indicated for the treatment of type 2 diabetes mellitus, offering convenient once-weekly administration to improve patient adherence [2,3]
- Favorable pharmacokinetic profile (long plasma half-life, high oral bioavailability, minimal metabolism) supports sustained DPP-4 inhibition for 7 days per dose [3]
- Low plasma protein binding, minimal drug-drug interaction potential, and low toxicity make it suitable for combination with other antidiabetic agents (e.g., metformin, SGLT2 inhibitors) [2,3]
- It is a natural-product-derived preclinical candidate, with preclinical data supporting clinical development and approval for type 2 diabetes treatment [3]

C22H26FN5O6

475.47

475.186

C, 55.57; H, 5.51; F, 4.00; N, 14.73; O, 20.19

1029877-94-8

Trelagliptin;865759-25-7

44183569

White to off-white solid powder

1.234

171.65

3

10

6

34

750

1

FC1C([H])=C([H])C(C#N)=C(C=1[H])C([H])([H])N1C(N(C([H])([H])[H])C(C([H])=C1N1C([H])([H])C([H])([H])C([H])([H])[C@]([H])(C1([H])[H])N([H])[H])=O)=O.O([H])C(C([H])([H])C([H])([H])C(=O)O[H])=O

OGCNTTUPLQTBJI-XFULWGLBSA-N

InChI=1S/C18H20FN5O2.C4H6O4/c1-22-17(25)8-16(23-6-2-3-15(21)11-23)24(18(22)26)10-13-7-14(19)5-4-12(13)9-20;5-3(6)1-2-4(7)8/h4-5,7-8,15H,2-3,6,10-11,21H2,1H3;1-2H2,(H,5,6)(H,7,8)/t15-;/m1./s1

2-[[6-[(3R)-3-aminopiperidin-1-yl]-3-methyl-2,4-dioxopyrimidin-1-yl]methyl]-4-fluorobenzonitrile;butanedioic acid

SYR-472; SYR 472; SYR472; TRELAGLIPTIN SUCCINATE; 1029877-94-8; Trelagliptin (succinate); Trelagliptin; Trelagliptin succinate; brand name: Zafatek

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，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)

配方 1 中的溶解度: ≥ 2.5 mg/mL (5.26 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 (5.26 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 (5.26 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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配方 4 中的溶解度: 50 mg/mL (105.16 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶.

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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。