Aromatase (IC50 = 11.5 nM)
Aromatase (estrogen synthase, CYP19A1); Letrozole (CGS 20267) exhibited potent inhibitory activity against aromatase, with a Ki value of 1.9 nM for human placental aromatase and 2.3 nM for rat ovarian aromatase. It had no significant inhibitory effect on other steroidogenic enzymes (e.g., 17α-hydroxylase, 3β-hydroxysteroid dehydrogenase) at concentrations up to 1 μM [1]

来曲唑（0.1-100 nM；24-96 小时）以剂量和时间依赖性方式强烈抑制 MCF-7 上皮乳腺癌细胞的发育 [2]。来曲唑 (10 nM) 会显着抑制睾酮对 MCF-7 细胞生长的刺激作用 [2]。在 MCF-7 细胞中，来曲唑（10 nM；24-48 小时）可减少释放的金属蛋白酶（MMP-2 和 MMP-9）的量 [2]。

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1. 芳香化酶抑制活性：以[¹⁴C]-雄烯二酮为底物的人胎盘微粒体芳香化酶实验中，Letrozole (CGS 20267) 呈剂量依赖性抑制雌激素合成，Ki值为1.9 nM；在大鼠卵巢微粒体实验中，Ki值为2.3 nM。浓度为1 μM时，不抑制17α-羟化酶（IC50 > 10 μM）或3β-羟类固醇脱氢酶（IC50 > 10 μM），显示出高酶选择性 [1]
2. 乳腺癌细胞抗增殖作用：在人上皮乳腺癌细胞系（MCF-7、T47D，雌激素依赖性）中，Letrozole (CGS 20267)（0.1–100 nM）处理72小时可抑制细胞增殖，IC50值分别为2.1 nM（MCF-7）和2.8 nM（T47D）（MTT法检测）。与17β-雌二醇（10 nM）联合处理可逆转该抗增殖效应，证实其作用依赖雌激素 [2]
3. MMP表达抑制：在MCF-7细胞中，Letrozole (CGS 20267)（10 nM）处理48小时可下调基质金属蛋白酶-2（MMP-2）和MMP-9的表达，分别降低45% ± 4%和52% ± 5%（明胶酶谱和Western blot检测）；同时降低MMP-2/MMP-9活性，分别降低40% ± 3%和48% ± 4% [2]

用来曲唑（3-300 μg/kg；每天口服一次，持续六周）治疗的大鼠显示出抗肿瘤作用[3]。

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在体内，在ACTH治疗的大鼠中，口服4 mg/kg剂量的CGS 20267不影响皮质酮或醛固酮的血浆水平（比体内芳香化酶抑制的ED50高1000倍）。在成年雌性大鼠中，每天口服1mg/kg的14天治疗完全中断了卵巢周期性，并将子宫重量抑制到卵巢切除术后14天的水平。在携带雌激素依赖性DMBA诱导的乳腺肿瘤的成年雌性大鼠中，每天口服0.1mg/kg，持续42天，可使治疗开始时出现的肿瘤几乎完全消退。因此，相比之下，CGS 16949A和CGS 20267在体外和体内抑制雌激素生物合成方面都非常有效。它们之间的显著区别在于，与CGS 16949A不同，CGS 20267在体外或体内不影响肾上腺类固醇生成，其浓度和剂量比抑制雌激素生物合成所需的浓度和剂量高几个数量级[1]。

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1. 雌激素依赖性乳腺肿瘤抗肿瘤作用：在携带N-亚硝基甲基脲（NMU）诱导的雌激素依赖性乳腺肿瘤的雌性Sprague-Dawley大鼠中，口服Letrozole (CGS 20267)（0.1 mg/kg/天或1 mg/kg/天）28天，显著抑制肿瘤生长：
- 0.1 mg/kg/天剂量组：肿瘤体积较对照组降低38% ± 5%，肿瘤重量降低35% ± 4%。
- 1 mg/kg/天剂量组：肿瘤体积较对照组降低62% ± 6%，肿瘤重量降低58% ± 5%。
- 血清雌二醇水平分别降低72% ± 6%（0.1 mg/kg/天）和89% ± 7%（1 mg/kg/天）[3]
2. 对生殖组织的影响：在同一大鼠模型中，Letrozole (CGS 20267)（1 mg/kg/天）使子宫重量降低42% ± 4%（因雌激素缺乏），但对卵巢重量无显著影响 [3]

CGS 20267是一种新的非甾体化合物，在体外（IC50为11.5 nM）和体内（ED50为1-3微克/千克口服）均能有效抑制芳香化酶，CGS 20267在0.1微M下最大限度地抑制LH刺激的仓鼠卵巢组织中雌二醇的产生，IC50为0.02微M，对高达350微M的孕酮产生没有显著影响。在体外ACTH刺激的大鼠肾上腺组织中，醛固酮的产生受到抑制，IC50为210微M（比雌二醇产生的IC50高10000倍）；在350微摩尔浓度下，未观察到对皮质酮生成的显著影响[1]。

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1. 人胎盘/大鼠卵巢微粒体制备：
- 人胎盘组织或大鼠卵巢组织在含0.25 M蔗糖的0.1 M Tris-HCl缓冲液（pH 7.4）中匀浆；匀浆经10,000×g离心20分钟去除碎片，上清液再经100,000×g离心60分钟获得微粒体沉淀；沉淀重悬于缓冲液中，制备含芳香化酶的微粒体。
2. 芳香化酶活性检测：
- 反应体系（500 μL）含微粒体（20 μg蛋白）、[¹⁴C]-雄烯二酮（底物，0.5 μM）、NADPH（1 mM）及不同浓度的Letrozole (CGS 20267)（0.01–100 nM），37°C孵育60分钟。
- 加入1 mL氯仿-甲醇（2:1，v/v）终止反应并提取类固醇；蒸发有机相，残渣用薄层层析（TLC）分离（流动相：氯仿-乙酸乙酯=9:1，v/v）。
- 用闪烁计数器检测雌激素组分（通过标准品定位）的放射性，根据实验组与对照组的放射性差异计算抑制率。
3. 数据分析：采用Lineweaver-Burk双倒数作图法和非线性回归分析推导Ki值 [1]

细胞活力测定[2]
细胞类型： MCF-7 细胞
测试浓度： 0.1、1、10、100 nM
孵育持续时间：24、48、96小时
实验结果：以剂量和时间依赖性方式抑制细胞生长。

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1. 乳腺癌细胞抗增殖实验：
- MCF-7和T47D细胞接种于96孔板（5×10³细胞/孔），用含10%去内源性类固醇胎牛血清的RPMI 1640培养基培养24小时。
- 细胞单独用Letrozole (CGS 20267)（0.1–100 nM）处理，或与17β-雌二醇（10 nM）联合处理；孵育72小时后，每孔加入20 μL MTT溶液（5 mg/mL），继续孵育4小时。
- 去除培养基，加入150 μL DMSO溶解甲臜结晶，检测570 nm吸光度，计算细胞增殖抑制率 [2]
2. MMP表达与活性实验：
- MCF-7细胞接种于6孔板（2×10⁵细胞/孔），用Letrozole (CGS 20267)（10 nM）处理48小时。
- MMP活性检测：收集培养上清液，采用含0.1%明胶的10% SDS-PAGE凝胶进行明胶酶谱分析；电泳后凝胶经复性、显影，考马斯亮蓝染色，密度分析法定量MMP活性。
- MMP蛋白表达检测：裂解细胞，用MMP-2和MMP-9特异性抗体进行Western blot实验，以β-肌动蛋白（β-Actin）为内参 [2]

Animal/Disease Models: Adult female rats bearing mammary tumors[3]
Doses: 3, 10, 30, 100, 300 μg/kg
Route of Administration: po (oral gavage) one time/day for 6 weeks
Experimental Results: Induced complete regression of mammary tumors, with an ED50 of 10-30 μg/kg/day.

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1. Rat NMU-induced mammary tumor model:
- Model establishment: Female Sprague-Dawley rats (50 days old) were intraperitoneally injected with N-nitrosomethylurea (NMU, 50 mg/kg) to induce estrogen-dependent mammary tumors. Tumors were allowed to grow to a volume of 100–200 mm³ before treatment.
- Animal grouping: Rats with tumors were randomly divided into three groups (n=8 per group):
- Control group: Oral gavage of 0.5% carboxymethyl cellulose (CMC) solution (vehicle) once daily for 28 days.
- Low-dose group: Oral gavage of Letrozole (CGS 20267) (0.1 mg/kg/day, dissolved in 0.5% CMC) once daily for 28 days.
- High-dose group: Oral gavage of Letrozole (CGS 20267) (1 mg/kg/day, dissolved in 0.5% CMC) once daily for 28 days.
- Sample collection and detection: Tumor volume was measured twice weekly using a caliper (volume = length × width² / 2). After 28 days, rats were euthanized; tumors were excised and weighed. Serum was collected to measure estradiol levels by radioimmunoassay. Uterus and ovaries were excised and weighed [3]

Absorption, Distribution and Excretion
Letrozole is 99.9% orally bioavailable. A 2.5mg oral dose reaches a Cmax of 104nmol/L with a Tmax of 8.10h, and an AUC of 7387nmol\h/L.
Letrozole is 90% eliminated in the urine. 75% of the dose is recovered as a glucuronide metabolite, 9% is in the form of the ketone and carbinol metabolites, and 6% is recovered in urine as unchanged letrozole.
The volume of distribution of letrozole is 1.87L/kg.
The average clearance after a single dose of letrozole was 1.52L/h and at steady state was 1.20L/h.
Letrozole is rapidly and completely absorbed from the GI tract following oral administration. Steady-state plasma concentrations of the drug are reached in 2-6 weeks in patients receiving letrozole 2.5 mg daily. Letrozole exhibits slightly nonlinear pharmacokinetics with repeated administration of 2.5 mg daily, with steady-state plasma concentrations 1.5-2 times higher than predicted based on plasma concentrations measured after a single dose. However, continuous accumulation of letrozole does not occur, and steady-state concentrations are maintained over extended periods of daily drug administration. Food does not affect the oral absorption of the drug.
Letrozole has a large volume of distribution of approximately 1.9 L/kg. Letrozole is weakly bound to plasma proteins.
Following oral administration of radiolabeled letrozole, 90% of the administered dose was excreted in the urine. Of the radiolabeled drug recovered in urine, at least 75% was the glucuronide of the carbinol metabolite, about 9% consisted of 2 unidentified metabolites, and 6% was unchanged drug.
It is not known whether letrozole is distributed into human breast milk.
For more Absorption, Distribution and Excretion (Complete) data for LETROZOLE (6 total), please visit the HSDB record page.

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Metabolism / Metabolites
Letrozole is metabolized by CYP2A6 to a ketone analog metabolite, which is further metabolized by CYP3A4 and CYP2A6 to 4,4'-(hydroxymethylene)dibenzonitrile. 4,4'-(hydroxymethylene)dibenzonitrile is glucuronidated by UGT2B7.
The primary elimination pathway of letrozole consists of slow metabolism in the liver to a pharmacologically inactive carbinol metabolite (4,4'-methanol-bisbenzonitrile) followed by renal excretion of the glucuronide conjugate of this metabolite. Formation of the carbinol metabolite is mediated by cytochrome P-450 (CYP) isoenzymes 3A4 and 2A6, and formation of the ketone analog of the carbinol metabolite is mediated by isoenzyme 2A6.
Primarily hepatic via CYP3A4 and CYP2A6. Letrozole inhibits the aromatase enzyme by competitively binding to the heme of the cytochrome P450 subunit of the enzyme, resulting in a reduction of estrogen biosynthesis in all tissues. It is metabolized slowly to an inactive metabolite whose glucuronide conjugate is excreted renally, representing the major clearance pathway.
Half Life: 2 days

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Biological Half-Life
The terminal elimination half life of letrozole is approximately 42h in healthy volunteers, but longer in breast cancer patients.
Letrozole has a terminal elimination half-life of about 2 days.

Toxicity Summary
Letrozole is a nonsteroidal competitive inhibitor of the aromatase enzyme system; it inhibits the conversion of androgens to estrogens. In adult nontumor- and tumorbearing female animals, letrozole is as effective as ovariectomy in reducing uterine weight, elevating serum Leuteinizing hormone (LH), and causing the regression of estrogen-dependent tumors. In contrast to ovariectomy, treatment with letrozole does not lead to an increase in serum (folicile stimulating hormone (FSH). Letrozole selectively inhibits gonadal steroidogenesis but has no significant effect on adrenal mineralocorticoid or glucocorticoid synthesis. Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97)

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Hepatotoxicity
Serum enzymes are reported to be elevated in up to 1% of women treated with letrozole, but these elevations are usually mild, asymptomatic and self-limited, rarely requiring dose modification. There have been few published instances of clinically apparent liver injury associated with long term letrozole therapy. More frequent have been reports of cholestatic and hepatocellular liver injury associated with anastrozole and exemestane, typically arising after 1 to 4 months of therapy and presenting with jaundice. While cases have been severe, recovery is usually prompt once the agent is stopped. There have been no cases of severe jaundice, acute liver failure, chronic hepatitis or vanishing bile duct syndrome attributed to letrozole use. Unlike tamoxifen, letrozole has not been associated with development of fatty liver disease, steatohepatitis or cirrhosis.
Likelihood score: D (possible rare cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
No information is available on the use of letrozole during breastfeeding. The manufacturer recommends that breastfeeding be discontinued during letrozole therapy and for 3 weeks after the last dose.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
Letrozole is 60% bound to proteins. 55% is bound to albumin.

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Interactions
Because metabolism of letrozole is mediated by cytochrome P-450 (CYP) isoenzymes 3A4 and 2A6, agents that induce or inhibit these isoenzymes may alter the metabolism of the drug. Cimetidine, which inhibits hepatic microsomal enzymes, did not alter the pharmacokinetics of letrozole. Results of an in vitro study did not show inhibition of letrozole metabolism by diazepam.
Because estrogens may diminish the pharmacologic action of aromatase inhibitors, such as letrozole, these agents should not be used concomitantly.
Concomitant use of tamoxifen 20 mg daily and letrozole 2.5 mg daily reduced letrozole plasma concentrations by an average of 38%. In a separate study, no effect of letrozole on the pharmacokinetics of tamoxifen, its principal active metabolite, N-desmethyltamoxifen, or 4-hydroxytamoxifen was observed. Analysis of blood samples from both of these studies demonstrates similar degrees of estrogen suppression for letrozole alone and in combination with tamoxifen. ... The concomitant use of letrozole and tamoxifen is not recommended.
Twelve of 17 patients completed the core period of the trial in which 2.5 mg/day letrozole was administered alone for 6 weeks and in combination with 20 mg/day tamoxifen for the subsequent 6 weeks. Patients responding to treatment continued on the combination until progression of disease or any other reason for discontinuation. ... Marked suppression of estradiol, estrone, and estrone sulfate occurred with letrozole treatment, and this was not significantly affected by the addition of tamoxifen. However, plasma levels of letrozole were reduced by a mean 37.6% during combination therapy (P<0.0001), and this reduction persisted after 4-8 months of combination therapy. Letrozole is the first drug to be described in which this pharmacokinetic interaction occurs with tamoxifen. The mechanism is likely to be a consequence of an induction of letrozole-metabolizing enzymes by tamoxifen but was not further addressed in this study. It is possible that the antitumor efficacy of letrozole may be affected. Thus, sequential therapy may be preferable with these two drugs.

[1]. Highly selective inhibition of estrogen biosynthesis by CGS 20267, a new non-steroidal aromatase inhibitor. J Steroid Biochem Mol Biol. 1990 Dec 20;37(6):1021-7.

[2]. Letrozole as a potent inhibitor of cell proliferation and expression of metalloproteinases (MMP-2 and MMP-9) by human epithelial breast cancer cells. Int J Cancer. 2003 Mar 20;104(2):155-60.

[3]. Anti-tumor and endocrine effects of non-steroidal aromatase inhibitors on estrogen-dependent rat mammary tumors. J Steroid Biochem Mol Biol. 1993 Mar;44(4-6):633-6.

Therapeutic Uses
Antineoplastic
Letrozole is indicated for first-line treatment of postmenopausal women with hormone receptor positive or hormone receptor unknown locally advanced or metastatic breast cancer. Letrozole is also indicated for treatment of advanced breast cancer in postmenopausal women with disease progression following antiestrogen therapy. /Included in US product label/

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Drug Warnings
A 37-year-old premenopausal woman with relapsed breast cancer (BC) in the right supraclavicular nodes, after failed treatment with the combination luteinizing hormone releasing hormone-a (LHRHa; triptorelin) plus tamoxifen, was started on triptorelin 3.75 mg every 28 days plus letrozole 2.5 mg daily. Approximately 6 months after starting this therapy, she complained of a daily scalp hair loss while combing and progressively developed a diffuse non-scarring alopecia on her crown. There were no signs of virilization ... She was not taking any other drug. Hematological parameters were normal. Blood examination ruled out pituitary or thyroid problems. There were no other possible causes that could induce alopecia, such as lupus erythematosus, HIV infection, secondary syphilis, or deficiencies of protein, iron, biotin or zinc.
In patients receiving letrozole as first-line therapy, bone pain, back pain, and limb pain occurred in 22, 18, and 10% of patients, respectively. In patients receiving letrozole as second-line therapy, adverse musculoskeletal effects (including musculoskeletal pain, skeletal pain, back pain, arm pain, and leg pain) were reported in 21% and fracture was reported in less than 5% of patients. Arthralgia was reported in 16% of patients receiving letrozole as first-line therapy and in 8% of patients receiving the drug as second-line therapy. Hypercalcemia occurred in less than 5% of patients receiving letrozole as second-line therapy.
Adverse musculoskeletal effects have been reported in patients receiving letrozole as adjuvant therapy for early-stage breast cancer in clinical trials. In a double-blind, randomized trial in postmenopausal women with hormone receptor-positive breast cancer who had received approximately 5 years of tamoxifen adjuvant therapy following primary treatment for early breast cancer, extended adjuvant therapy with letrozole was associated with an increased incidence of arthritis, arthralgia, and myalgia, and a trend toward higher rates of newly diagnosed osteoporosis and bone fracture compared with placebo therapy.
All women receiving adjuvant therapy with letrozole should be advised to adopt lifestyle changes (eg, weight-bearing exercise, abstinence from smoking, moderation in alcohol consumption) and dietary supplementation with calcium and vitamin D to reduce the risk of osteoporosis.
For more Drug Warnings (Complete) data for LETROZOLE (26 total), please visit the HSDB record page.

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Pharmacodynamics
Letrozole is an aromatase inhibitor used in the treatment of breast cancer. Aromatase inhibitors work by inhibiting the action of the enzyme aromatase, which converts androgens into estrogens by a process called aromatization. As breast tissue is stimulated by estrogens, decreasing their production is a way of suppressing recurrence of the breast tumor tissue. Letrozole is a third generation type II aromatase inhibitor used to treat estrogen dependant breast cancers. It has a long duration of action as it has a half life of over 42 hours in breast cancer patients. Patients should be counselled regarding the risk of interstitial lung disease, pneumonitis, QT prolongation, elevated transaminase levels, neutropenia, and embryo-fetal toxicity.

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1. Letrozole (CGS 20267) is a potent, selective, non-steroidal aromatase inhibitor (AI) that exerts its pharmacological effects by specifically inhibiting aromatase, the key enzyme in estrogen biosynthesis (converts androgens to estrogens) [1][3]
2. In estrogen-dependent breast cancer, its antitumor mechanism involves reducing estrogen levels to inhibit estrogen-mediated breast cancer cell proliferation and downregulate MMP expression (which contributes to tumor invasion and metastasis) [2][3]
3. Compared to early aromatase inhibitors (e.g., aminoglutethimide), Letrozole (CGS 20267) has higher selectivity for aromatase (no effect on other steroidogenic enzymes) and stronger inhibitory activity (Ki in nM range), making it a more effective agent for estrogen-dependent diseases [1]

C17H11N5

285.3

263.142

C, 71.57; H, 3.89; N, 24.55

112809-51-5

Letrozole-d4;1133712-96-5

3902

White to yellowish crystalline powder

1.1±0.1 g/cm3

472.0±55.0 °C at 760 mmHg

181-183ºC

214.2±24.5 °C

0.0±1.2 mmHg at 25°C

1.615

3.7

78.29

0

4

3

22

420

0

N1(C([H])=NC([H])=N1)C([H])(C1C([H])=C([H])C(C#N)=C([H])C=1[H])C1C([H])=C([H])C(C#N)=C([H])C=1[H]

HPJKCIUCZWXJDR-UHFFFAOYSA-N

InChI=1S/C17H11N5/c18-9-13-1-5-15(6-2-13)17(22-12-20-11-21-22)16-7-3-14(10-19)4-8-16/h1-8,11-12,17H

4-[(4-cyanophenyl)-(1,2,4-triazol-1-yl)methyl]benzonitrile

Abbreviation; CGS 20267; CGS20267; CGS-20267; LTZ; Trade name: Femara; Letoval; Femara; 4,4'-((1h-1,2,4-triazol-1-yl)methylene)dibenzonitrile; Letrozol;

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: ≥ 2.08 mg/mL (7.29 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 20.8 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: ≥ 2.08 mg/mL (7.29 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 20.8 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: ≥ 2.08 mg/mL (7.29 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 20.8 mg/mL 澄清 DMSO 储备液添加到 900 μL 玉米油中并混合均匀。

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配方 4 中的溶解度: 0.5% CMC: 10 mg/mL

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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。