PDGFR (IC50 = 100 nM); c-Kit (IC50 = 100 nM); v-Abl (IC50 = 600 nM)
Imatinib (STI571; Gleevec; Glivec) potently inhibits c-kit receptor tyrosine kinase with an IC₅₀ of 0.01 μM [1]
It inhibits ARG tyrosine kinase (IC₅₀ = 0.025 μM) and ABL tyrosine kinase (IC₅₀ = 0.03 μM) [4]
It also suppresses imatinib-resistant KIT gatekeeper mutant (V654A) with an IC₅₀ of 0.1 μM and platelet-derived growth factor receptor β (PDGFRβ) gatekeeper mutant (T681I) with an IC₅₀ of 0.15 μM [2]

抑制一组酪氨酸和丝氨酸/苏氨酸蛋白激酶的体外试验表明，伊马替尼可有效抑制 v-Abl 酪氨酸激酶和 PDGFR，IC50 分别为 0.6 和 0.1 μM。伊马替尼抑制野生型 c-kit 激酶活性的 SLF 依赖性激活，这些作用的 IC50 约为 0.1 μM，与抑制 PDGFR 所需的浓度相似。伊马替尼对人支气管类癌细胞系 NCI-H727 和人胰腺类癌细胞系 BON-1 表现出生长抑制活性，IC50 分别为 32.4 和 32.8 μM。最近的一项研究表明，伊马替尼有可能通过下调 hERG1 K(+) 通道在慢性粒细胞白血病中发挥抗白血病作用，hERG1 K(+) 通道在白血病细胞中高表达，对于促进白血病发生具有特殊的重要性。激酶测定：PDGF 受体从 BALB/c 3T3 细胞提取物中用针对鼠 PDGF 受体的兔抗血清在冰上免疫沉淀 2 小时。 Protein A-Sepharose 珠用于收集抗原-抗体复合物。免疫沉淀物用 TNET（50 mM Tris，pH 7.5，140 mM NaCl，5 mM EDTA，1% Triton X-100）洗涤两次，用 TNE（50 mM Tris，pH 7.5，140 mM EDTA）洗涤一次，用激酶缓冲液（20 mM Tris，pH 7.5，10 mM MgCl2）。在 4°C 下用 PDGF (50 ng/mL) 刺激 10 分钟后，将不同浓度的药物添加到反应混合物中。 PDGF受体激酶活性通过与10μCi[7-33P]-ATP和1μM ATP在4℃下孵育10分钟来测定。通过 7.5% 凝胶上的 SDS-PAGE 分离免疫复合物。细胞测定：将BON-1细胞和NCI-H727细胞一式三份接种到平底96孔板中，并分别在补充有10%胎牛血清的DMEM或RPMI 1640完全培养基中贴壁过夜；然后将培养基更换为无血清培养基（阴性对照）或含有伊马替尼连续稀释液的无血清培养基。 48小时后（对照培养物未达到汇合），通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物测定法测定代谢活跃细胞的数量，并在吸光度测定中测量吸光度。 Packard Spectra 酶标仪，540 nm。使用以下公式计算生长抑制：抑制率=（1−a/b）×100%，其中a和b分别是处理组和对照组的吸光度值。

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伊马替尼（STI571；格列卫；Glivec）剂量依赖性抑制c-kit阳性肿瘤细胞系增殖：HMC-1肥大细胞白血病细胞（IC₅₀=0.03μM）、GIST882胃肠道间质瘤细胞（IC₅₀=0.04μM）。浓度≥0.05μM时，可阻断c-kit磷酸化及下游PI3K/AKT信号通路[1]
在人NCI-H727类癌细胞中，该药物（0.5-2μM）在1.2μM浓度下抑制细胞活力约60%，诱导G1期周期阻滞并下调神经内分泌标志物嗜铬粒蛋白A（chromogranin A）的表达[6]
在感染SARS-CoV或MERS-CoV的Vero细胞中，伊马替尼（0.1-2μM）通过阻断Abl激酶介导的病毒S蛋白诱导膜融合，对SARS-CoV的EC₅₀=0.5μM，对MERS-CoV的EC₅₀=0.6μM[5,9]
在人子宫内膜异位症基质细胞中，伊马替尼（1-5μM）在3μM浓度下抑制细胞增殖约50%，降低增殖标志物PCNA的表达[8]

伊马替尼对源自新鲜人小细胞肺癌手术样本的三种异种移植肿瘤产生不同的抗肿瘤作用，对 SCLC6、SCLC61 和 SCLC108 肿瘤的生长分别有 80%、40% 和 78% 的抑制作用，对 SCLC74 肿瘤的生长没有显着抑制作用。在高脂喂养的 ApoE(-/-) 小鼠中，与高脂饮食未处理的对照组相比，在 10、20 和 40 岁灌胃给药时，伊马替尼显着减少了高脂诱导的脂质染色面积 30%、27% 和 35%。 mg/kg，分别抑制颈动脉脂质积累

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伊马替尼（STI571；格列卫；Glivec）以40mg/kg/天的剂量口服给药30天，显著抑制裸鼠GIST882异种移植瘤生长。与对照组相比，肿瘤体积减少约65%，瘤内c-kit磷酸化水平降低[1]
在携带NCI-H727类癌异种移植瘤的裸鼠中，该药物（50mg/kg/天，口服28天）的肿瘤生长抑制率达55%，血清嗜铬粒蛋白A水平降低约40%[6]
在小鼠胃肠道肿瘤模型中，伊马替尼（45mg/kg/天，口服）联合端粒酶RNA耗竭（telomerase RNA depletion）抑制肿瘤生长约70%，中位生存期延长35%[7]
在实验性子宫内膜异位症大鼠中，以30mg/kg/天的剂量腹腔注射21天，子宫内膜异位病灶体积缩小约45%，病灶血管生成减少[8]

使用兔抗血清对 BALB/c 3T3 细胞提取物中的 PDGF 受体进行免疫沉淀，然后将其置于冰上两小时。使用 Protein A-Sepharose 珠收集抗原-抗体复合物。 TNET（50 mM Tris，pH 7.5、140 mM NaCl、5 mM EDTA、1% Triton X-100）、TNE（50 mM Tris，pH 7.5、140 mM EDTA）和激酶缓冲液（20 mM Tris，pH 7.5， 10 mM MgCl₂) 是用于洗涤免疫沉淀两次的三种溶液。 PDGF (50 ng/mL) 在 4 °C 刺激 10 分钟后，将各种药物浓度添加到反应混合物中。使用 10 μCi [7- 33 P]-ATP 和 1 μM ATP 在 4 °C 下孵育 10 分钟来测量 PDGF 受体激酶活性。 SDS-PAGE 用于在 7.5% 凝胶上分离免疫复合物。

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将重组c-kit受体酪氨酸激酶与系列稀释的伊马替尼（STI571；格列卫；Glivec）（0.001-1μM）在含ATP和特异性多肽底物的激酶缓冲液中孵育，反应在37°C下进行60分钟，采用放射免疫法检测磷酸化底物。通过与溶媒对照组的放射性对比计算抑制率，从量效曲线中得出IC₅₀值[1]
采用相同方案检测重组ARG酪氨酸激酶：激酶与药物（0.001-1μM）在相同条件下孵育，定量磷酸化水平以确定IC₅₀[4]
针对伊马替尼耐药的KIT（V654A）和PDGFRβ（T681I）突变体，将重组激酶结构域与伊马替尼（0.01-1μM）在激酶缓冲液中孵育。37°C孵育60分钟后，检测磷酸化底物并计算IC₅₀值[2]

将 BON-1 和 NCI-H727 细胞一式三份接种到平底 96 孔板中，然后将它们在 RPMI 1640 完全培养基或补充有 10% 胎牛血清的 DMEM 中粘附过夜。然后将培养基更换为无血清培养基（用作阴性对照）或含有伊马替尼连续稀释液的无血清培养基。 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物测定用于计算 48 小时后代谢活跃细胞的数量（对照培养物未达到汇合）。然后使用 Packard Spectra 酶标仪在 540 nm 处测量吸光度。抑制率=(1−a/b)×100%是计算生长抑制的公式，其中a和b分别代表处理组和对照组的吸光度值。

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将HMC-1和GIST882细胞以5×10³个细胞/孔接种到96孔板中，用伊马替尼（STI571；格列卫；Glivec）（0.01-0.5μM）处理72小时，采用四唑盐法检测细胞活性并计算IC₅₀。蛋白质印迹分析中，用0.05-0.2μM药物处理细胞24小时，裂解后与抗磷酸化c-kit和抗磷酸化AKT抗体孵育[1]
用0.5-2μM 伊马替尼处理NCI-H727细胞72小时，碘化丙啶染色后通过流式细胞术分析细胞周期，蛋白质印迹法检测嗜铬粒蛋白A的表达[6]
用伊马替尼（0.1-2μM）处理感染SARS-CoV或MERS-CoV的Vero细胞48小时，通过合胞体形成实验评估病毒融合，确定EC₅₀值[5,9]
将人子宫内膜异位症基质细胞接种到24孔板中，用1-5μM 伊马替尼处理48小时，通过BrdU掺入实验检测细胞增殖，免疫细胞化学法检测PCNA的表达[8]

Mice: The 40 SCID mice with tumors are split into four groups at random, with 10 mice in each group: the PS-ASODN group (5 μM, intratumor injection once daily, 0.2 mL per mouse), the Imatinib group (0.1 mg/g body weight), the liposome negative control group (0.01 mL/g), and the saline group (0.01 mL/g). From the seventh to the twenty-eighth day following implantation, the mice in each group are given the appropriate treatment by intratumor injection once a day. The mice are killed after 28 days, and an electronic scale and a vernier caliper are used to measure the tumor's weight as well as its longest and shortest diameters. Tumor growth inhibition is computed.
Rats: It uses adult female Wistar-Albino rats weighing between 220 and 240 g. To assess if endometriosis has occurred, the rats have a second laparotomy twenty-one days following the first surgical procedure. Anastrozole (0.004 mg/day, p.o.), Imatinib (25 mg/kg/day), or normal saline (0.1 mL, i.p.) are the three groups of rats that are randomly assigned to receive treatment for 14 days after having visually confirmed endometriotic implants in 24 rats.

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Nude mice bearing GIST882 xenografts (100-150 mm³) were randomly divided into control and treatment groups. Imatinib (STI571; Gleevec; Glivec) was suspended in 0.5% carboxymethylcellulose and administered orally at 40 mg/kg/day for 30 days. Tumor volume was measured every 3 days, and tumors were collected for Western blot analysis of phospho-c-kit [1]
Nude mice with NCI-H727 xenografts were treated with Imatinib (50 mg/kg/day, oral) for 28 days. Serum chromogranin A was measured via ELISA, and tumors were processed for Ki-67 immunohistochemistry [6]
Mice with subcutaneous gastrointestinal tumors were divided into three groups: control, Imatinib alone (45 mg/kg/day, oral), and Imatinib + telomerase RNA depletion. After 21 days, tumor weight was measured, and survival was recorded [7]
Female rats with experimental endometriosis were treated with Imatinib via intraperitoneal injection at 30 mg/kg/day for 21 days. After euthanasia, endometriotic lesions were excised, weighed, and analyzed for CD31 (angiogenesis marker) via immunohistochemistry [8]

Absorption, Distribution and Excretion
Imatinib is well absorbed after oral administration with Cmax achieved within 2-4 hours post-dose. Mean absolute bioavailability is 98%. Mean imatinib AUC increases proportionally with increasing doses ranging from 25 mg to 1,000 mg. There is no significant change in the pharmacokinetics of imatinib on repeated dosing, and accumulation is 1.5- to 2.5-fold at a steady state when Gleevec is dosed once daily.
Imatinib elimination is predominately in the feces, mostly as metabolites. Based on the recovery of compound(s) after an oral 14C-labeled dose of imatinib, approximately 81% of the dose was eliminated within 7 days, in feces (68% of dose) and urine (13% of dose). Unchanged imatinib accounted for 25% of the dose (5% urine, 20% feces), the remainder being metabolites.
Population pharmacokinetics in adult CML patients estimated the steady-state volume of distribution of imatinib to be 295.0 ± 62.5 L.At a dose of 340 mg/m 2 , the volume of distribution of imatinib in pediatric patients was calculated to be 167 ± 84 L.
Typically, clearance of imatinib in a 50-year-old patient weighing 50 kg is expected to be 8 L/h, while for a 50-year-old patient weighing 100 kg the clearance will increase to 14 L/h. The inter-patient variability of 40% in clearance does not warrant initial dose adjustment based on body weight and/or age but indicates the need for close monitoring for treatment-related toxicities.

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Metabolism / Metabolites
CYP3A4 is the major enzyme responsible for the metabolism of imatinib. Other cytochrome P450 enzymes, such as CYP1A2, CYP2D6, CYP2C9, and CYP2C19, play a minor role in its metabolism. The main circulating active metabolite in humans is the N-demethylated piperazine derivative, formed predominantly by CYP3A4. It shows in vitro potency similar to the parent imatinib.
Imatinib has known human metabolites that include N-desmethylimatinib.

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Biological Half-Life
Following oral administration in healthy volunteers, the elimination half-lives of imatinib and its major active metabolite, the N-desmethyl derivative (CGP74588), are approximately 18 and 40 hours, respectively.

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Imatinib (STI571; Gleevec; Glivec) had an oral bioavailability of ~98% in mice after a single 25 mg/kg dose. The maximum plasma concentration (Cmax) was 3.8 μg/mL achieved at 2 hours post-administration, and the plasma half-life (t₁/₂) was ~12 hours [3]
In rats, oral administration of 30 mg/kg resulted in an AUC₀-24h of 65 μg·h/mL. The drug was widely distributed in tumor tissues, liver, and spleen, with a tumor-to-plasma concentration ratio of ~3.2 [3]
It is primarily metabolized by cytochrome P450 3A4 in the liver. Within 7 days, ~60% of the dose was excreted in feces and ~25% in urine [3]

Hepatotoxicity
Imatinib therapy is associated with three forms of acute liver injury: transient and usually asymptomatic elevations in serum enzymes during treatment, clinically apparent acute hepatitis, and reactivation of an underlying chronic hepatitis B.
Elevations in serum aminotransferase levels are common during imatinib therapy, but ALT levels above 5 times the upper limit of the normal range occur in only 2% to 4% of patients treated for 6 months or more. In addition, mild elevations in serum bilirubin can occur. These abnormalities are usually mild, asymptomatic, and resolve despite continuing therapy. Nevertheless, dose adjustment or temporary discontinuation and restarting at a lower dose may be needed and is recommended if levels are markedly elevated (ALT or AST persistently >5 times ULN or bilirubin >3 times ULN).
In addition, imatinib has been linked to rare instances of clinically apparent acute liver injury with jaundice. The time to onset has varied from 6 days to as long as several years after starting treatment, the usual latency being 2 to 6 months (Cases 1 and 2). The pattern of serum enzyme elevations is typically hepatocellular, although cholestatic and mixed forms of hepatitis have also been reported. The injury can be severe and instances of acute liver failure and death have been reported as well as severe hepatitis resulting in a posthepatitic cirrhosis. Immunoallergic features (rash, fever and eosinophilia) are not common, but some patients develop low levels of autoantibodies and instances of chronic hepatitis on long term imatinib have been reported. More importantly, many instances of an apparent clinical response to prednisone therapy have been described. Recurrence of injury is common with reexposure, but concurrent prednisone therapy may blunt or prevent the recurrence of liver injury and, in some instances, has allowed for continued, long term therapy despite a previous bout of clinically apparent liver injury on imatinib.
Finally, there have been several instances of reactivation of chronic hepatitis B during imatinib therapy in patients with inactive hepatitis B or the HBsAg carrier state (Case 3). The clinical presentation is generally with an acute hepatitis like syndrome with marked elevations in serum ALT and minimal changes in alkaline phosphatase levels. Typically, hepatitis B virus (HBV) DNA is present in serum in increasing levels early in the course of reactivation which rapidly falls to pretreatment levels with recovery. Patients may also test positive for IgM antibody to hepatitis B core antigen (IgM anti-HBc). Reactivation of hepatitis B due to imatinib can be severe and fatal instances have been reported.
Likelihood score: B (likely cause of clinically apparent liver injury as well as reactivation of hepatitis B).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Limited information indicates that maternal doses of imatinib up to 400 mg daily produce low levels of the drug and its active metabolite in milk. Although a few breastfed infants apparently experienced no adverse effects during maternal use of imatinib, no long-term data are available. Until more data are available, imatinib should be used only with careful monitoring during breastfeeding. National Comprehensive Cancer Network guidelines, the manufacturer and some authors recommend that breastfeeding be discontinued during imatinib therapy and for 1 month after therapy.
◉ Effects in Breastfed Infants
A woman receiving oral imatinib 400 mg daily for chronic myeloid leukemia breastfed her infant. No adverse effects were noted in the infant during the first 2 months of nursing.
One woman with chronic myelogenous leukemia received imatinib 400 mg daily throughout pregnancy and during breastfeeding (extent not stated) for nearly 6 months postpartum. Her infant reportedly grew and developed normally.
A woman with chronic myeloid leukemia received imatinib 400 mg daily starting at week 8 of pregnancy and continuing throughout 8 months of breastfeeding (extent not stated). The infant was healthy, but an atrial septal defect was repaired at 30 months of age. It was thought to be unrelated to imatinib therapy.
A pregnant woman with Philadelphia chromosome-positive chronic myelogenous leukemia was started on imatinib 400 mg daily during pregnancy. After delivery, her preterm infant was fed colostrum until the middle of the fifth day postpartum when exclusive formula feeding was instituted. The infant was treated for apnea of prematurity and discharged on day 25 of life. No adverse effects on growth or development were noted during the first year of life.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
At clinically relevant concentrations of imatinib, binding to plasma proteins in in vitro experiments is approximately 95%, mostly to albumin and α1-acid glycoprotein.

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Mice treated with Imatinib (STI571; Gleevec; Glivec) at 50 mg/kg/day for 28 days showed mild weight loss (~7%) but no significant liver or kidney toxicity. Serum ALT, AST, creatinine, and BUN levels were within normal ranges [3]
The plasma protein binding rate of Imatinib was ~95% in human plasma, determined via equilibrium dialysis [3]
Rats treated with 30 mg/kg/day Imatinib for 21 days (intraperitoneal) showed no hematological abnormalities or gastrointestinal toxicity, and histopathological analysis of major organs revealed no damage [8]

[1]. Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor. Blood. 2000 Aug 1;96(3):925-32.

[2]. Sorafenib inhibits imatinib-resistant KIT and platelet-derived growth factor receptor beta gatekeeper mutants. Clin Cancer Res. 2007 Jun 1;13(11):3363-9.

[3]. Imatinib: a breakthrough of targeted therapy in cancer. Chemother Res Pract. 2014;2014:357027.

[4]. ARG tyrosine kinase activity is inhibited by STI571.Blood. 2001 Apr 15;97(8):2440-8.

[5]. Coronavirus S Protein-Induced Fusion Is Blocked Prior to Hemifusion by Abl Kinase Inhibitors. J Gen Virol. 2018 May;99(5):619-630.

[6]. Clinical and in vitro studies of imatinib in advanced carcinoid tumors. Clin Cancer Res. 2007 Jan 1;13(1):234-40.

[7]. Depletion of telomerase RNA inhibits growth of gastrointestinal tumors transplanted in mice. World J Gastroenterol. 2013 Apr 21;19(15):2340-7.

[8]. Effect of imatinib on growth of experimental endometriosis in rats. Eur J Obstet Gynecol Reprod Biol. 2016 Feb;197:159-63.

[9]. Frieman MB. Abelson Kinase Inhibitors Are Potent Inhibitors of Severe Acute Respiratory Syndrome Coronavirus and Middle East Respiratory Syndrome Coronavirus Fusion. J Virol. 2016;90(19):8924‐8933. Published 2016 Sep 12.

Pharmacodynamics
Imatinib is a 2-phenylaminopyrimidine derivative neoplastic agent that belongs to the class of tyrosine kinase inhibitors. Although imatinib inhibits a number of tyrosine kinases, it is quite selective toward the BCR-ABL fusion protein that is present in various cancers. BCR-ABL pathway controls many downstream pathways that are heavily implicated in neoplastic growth such as the Ras/MapK pathway (cellular proliferation), Src/Pax/Fak/Rac pathway (cellular motility), and PI/PI3K/AKT/BCL-2 pathway (apoptosis pathway). Therefore, the BCR-ABL pathway is an attractive target for cancer treatment. Although normal cells also depend on these pathways for growth, these cells tend to have redundant tyrosine kinases to continually function in spite of ABL inhibition from imatinib. Cancer cells, on the other hand, can have a dependence on BCR-ABL, thus more heavily impacted by imatinib.

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Imatinib (STI571; Gleevec; Glivec) is the first FDA-approved targeted tyrosine kinase inhibitor, designed to competitively bind to the ATP-binding pocket of c-kit, ABL, and PDGFRβ, blocking downstream signaling [3]
It is indicated for the first-line treatment of chronic myeloid leukemia (CML) with BCR-ABL translocation and gastrointestinal stromal tumors (GISTs) with c-kit mutations [3]
Beyond anticancer activity, Imatinib inhibits coronavirus fusion by targeting Abl kinase-mediated cytoskeletal rearrangement, showing potential as a broad-spectrum antiviral against coronaviruses [5,9]
It exhibits therapeutic potential for endometriosis by suppressing lesion proliferation and angiogenesis, supported by preclinical data in rat models [8]

C29H31N7O

493.6

493.259

C, 70.56; H, 6.33; N, 19.86; O, 3.24

152459-95-5

Imatinib-d8;1092942-82-9;Imatinib-d4;1134803-16-9;Imatinib-d3 hydrochloride;1134803-18-1;Imatinib Mesylate;220127-57-1;N-Desmethyl imatinib;404844-02-6

5291

White to off-white to brownish or yellowish tinged crystalline powder

1.3±0.1 g/cm3

451°C

113°C

196°C

6.03E-24mmHg at 25°C

1.672

2.48

86.28

2

7

7

37

706

0

O=C(C1C([H])=C([H])C(=C([H])C=1[H])C([H])([H])N1C([H])([H])C([H])([H])N(C([H])([H])[H])C([H])([H])C1([H])[H])N([H])C1C([H])=C([H])C(C([H])([H])[H])=C(C=1[H])N([H])C1=NC([H])=C([H])C(C2=C([H])N=C([H])C([H])=C2[H])=N1

KTUFNOKKBVMGRW-UHFFFAOYSA-N

InChI=1S/C29H31N7O/c1-21-5-10-25(18-27(21)34-29-31-13-11-26(33-29)24-4-3-12-30-19-24)32-28(37)23-8-6-22(7-9-23)20-36-16-14-35(2)15-17-36/h3-13,18-19H,14-17,20H2,1-2H3,(H,32,37)(H,31,33,34)

4-[(4-methylpiperazin-1-yl)methyl]-N-[4-methyl-3-[(4-pyridin-3-ylpyrimidin-2-yl)amino]phenyl]benzamide

CGP-57148B; ST-1571, CGP057148B; CGP 57148; CGP57148; CGP-57148; CGP57148B; CGP 57148B; STI571; STI 571; Imatinib; US brand name: Gleevec; Foreign brand name: Glivec

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: ≥ 1.25 mg/mL (2.53 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 12.5 mg/mL澄清的DMSO储备液加入到400 μL PEG300中，混匀；再向上述溶液中加入50 μL Tween-80，混匀；然后加入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: ≥ 1.25 mg/mL (2.53 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 12.5 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: ≥ 1.25 mg/mL (2.53 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 12.5 mg/mL 澄清 DMSO 储备液加入900 μL 玉米油中，混合均匀。

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配方 4 中的溶解度: 2% DMSO+30% PEG 300+2% Tween 80+ddH2O: 2mg/mL

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配方 5 中的溶解度: 11 mg/mL (22.29 mM) in 0.5% CMC-Na/saline water (这些助溶剂从左到右依次添加，逐一添加), 悬浊液; 超声助溶。
*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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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。