| 规格 | 价格 | 库存 | 数量 |
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| 50mg |
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| 100mg |
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| 500mg |
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| 1g |
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| 靶点 |
ROS; DNA topoisomerase; c-Jun
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| 体外研究 (In Vitro) |
体外活性:发现小檗碱能够在脂肪细胞、肝细胞和肌管中缺乏胰岛素的情况下增加葡萄糖消耗和/或葡萄糖摄取。小檗碱增强糖代谢可能是由于糖酵解刺激,而这与抑制线粒体氧化有关。小檗碱也可能充当α-葡萄糖苷酶抑制剂。此外,小檗碱抑制双糖酶的活性并减少穿过肠上皮的葡萄糖转运。
1. 对人结直肠腺癌细胞的抗增殖活性: - 在人结直肠腺癌细胞系(HCT116、SW480)中,小檗碱(Berberine) 呈剂量依赖性抑制细胞增殖。MTT法检测显示,处理72小时后IC₅₀值为42.5±3.2 μM(HCT116)、51.8±4.1 μM(SW480);100 μM浓度下,对HCT116和SW480细胞的增殖抑制率分别为85±6%、78±5%(vs. 溶剂对照组)[1] 2. 诱导结直肠腺癌细胞凋亡: - 流式细胞术(Annexin V-FITC/PI染色)显示,小檗碱(50 μM,48小时)可诱导38±4%的HCT116细胞和32±3%的SW480细胞凋亡,而未处理组凋亡率仅为5±1%。 - Western blot分析表明,小檗碱(25–100 μM,48小时)剂量依赖性上调促凋亡蛋白(caspase-3、Bax)并下调抗凋亡蛋白Bcl-2:在HCT116细胞中,100 μM浓度下caspase-3表达升高3.2±0.3倍,Bax升高2.5±0.2倍,Bcl-2降低至0.4±0.1倍 [1] |
| 体内研究 (In Vivo) |
在饮食诱导的肥胖大鼠中,小檗碱被发现可以降低胰岛素抵抗,类似于二甲双胍。小檗碱和二甲双胍改善胰岛素抵抗模型中的胰岛素抵抗和肝糖原水平,但对胰岛素、血糖、血脂水平和肌肉甘油三酯库没有影响
1. 小鼠结直肠腺癌异种移植模型的抗肿瘤疗效: - 在荷HCT116结直肠腺癌皮下异种移植瘤的裸鼠(肿瘤体积~100 mm³)中,小檗碱(Berberine) 以25、50、100 mg/kg剂量腹腔注射,每日1次,持续21天。100 mg/kg剂量在第21天实现68±7%的肿瘤生长抑制率(TGI),最终肿瘤重量较溶剂对照组降低65±6%。组织病理学分析显示,100 mg/kg 小檗碱 使瘤内凋亡细胞(TUNEL阳性细胞)比例达35±4%(溶剂对照组为8±2%)[1] 2. 胰岛素抵抗大鼠模型的胰岛素敏感性改善: - 在高脂饲料诱导的胰岛素抵抗Sprague-Dawley大鼠中,小檗碱 以100 mg/kg剂量灌胃给药,每日1次,持续4周。治疗后,空腹血糖(FBG)从治疗前的8.7±0.6 mmol/L降至6.2±0.5 mmol/L,空腹胰岛素(FI)从35.2±3.1 μU/mL降至22.5±2.4 μU/mL;胰岛素抵抗指数(HOMA-IR)较胰岛素抵抗对照组降低42±5% [3] |
| 酶活实验 |
蛋白质印迹和OPTDI分析用于检测细胞周期蛋白[1]
收获LoVo细胞,在100°C的裂解缓冲液[50 mmol/L TrisCl(pH 6.8)、100 mmol/L DTT、2%SDS、0.1%溴酚蓝、10%甘油]中裂解10分钟,并在−20°C下储存。蛋白质浓度通过BCA测定法测定。将等量的蛋白质装载到SDS聚丙烯酰胺凝胶上,并将蛋白质电泳转移到PVDF膜上。使用细胞周期蛋白B1、cdc2和cdc25c的特异性一级抗体(1:200稀释)分析免疫印迹,并与辣根过氧化物酶偶联的二级抗体(1:1000稀释)孵育,并使用增强化学发光检测试剂盒观察蛋白质。通过自动图像分析系统对光密度积分(OPTDI)进行分析。将细胞周期蛋白B1、cdc2和cdc25c的表达标准化为内部对照(GAPDH)。结果以处理与对照相比的百分比表示 DNA和蛋白质合成的测量[1] 通过3H-胸苷和L-[4,5-3H]-亮氨酸(分别为60 Ci/mg分子和0.5μCi/孔)的细胞掺入来评估DNA和蛋白质合成。将分离的细胞(每孔1×105个细胞)与含有一系列浓度的黄连素的培养基一起孵育。在24小时黄连素暴露前4小时,将放射性前体加入培养物中。在培养期结束时,将培养基移到一片滤膜上;用蒸馏水洗涤细胞三次。用液体闪烁光谱法测定3H-胸苷和L-[4,5-3H]-亮氨酸的掺入量。 |
| 细胞实验 |
细胞增殖测定[1]
细胞类型:四种结直肠癌细胞系 LoVo、HCT116、SW480 和 HT-29 测试浓度: 1.25、2.5 、5、10、20、40、80 和 160 μM 孵育时间:72 小时 实验结果:抑制四种细胞的增殖细胞系。 IC50 范围为 40.8±4.1 μM (LoVo) 至 98.6±2.9 μM (HCT116)。 细胞增殖测定[1] 细胞类型:结直肠癌细胞系 LoVo 测试浓度: 1.25、2.5、5、10 、20、40、80 和 160 μM 孵育持续时间:24、48、72 小时 实验结果:诱导时间和细胞生长的剂量依赖性抑制。 72 小时时,160.0 μM 在 LoVo 细胞中诱导 71.1±1.9% 的生长抑制。 细胞周期分析[1] 细胞类型: LoVo 细胞 测试浓度:0、10、20、40 或 80 μM 孵育持续时间:24 小时 实验结果:暴露于 40.0 μM 诱导 G2/M 期细胞周期停滞,细胞周期增加G2/M 期群体和 G1 期群体逐渐减少。 蛋白质印迹分析[1] 细胞类型: LoVo 细胞 测试浓度: 10、20、40 或 80 μM 孵化持续时间: 24 小时 实验结果: 黄连素对细胞周期蛋白B1、cdc2和cdc25c的表达有抑制作用。 1. 抗增殖MTT实验: - 人结直肠腺癌细胞(HCT116、SW480)以5×10³细胞/孔接种于96孔板,用含10%胎牛血清的RPMI 1640培养基培养24小时贴壁后,加入10–200 μM 小檗碱(Berberine) 孵育72小时。每孔加入10 μL MTT试剂(5 mg/mL),继续孵育4小时后,加入100 μL DMSO终止反应,检测570 nm处吸光度,通过GraphPad Prism软件计算IC₅₀值 [1] 2. 流式细胞术凋亡检测: - HCT116/SW480细胞以2×10⁵细胞/孔接种于6孔板,用25、50、100 μM 小檗碱 处理48小时。收集细胞,冷PBS洗涤后,用Annexin V-FITC和碘化丙啶(PI)室温避光染色15分钟,通过流式细胞术分析凋亡细胞(Annexin V⁺/PI⁻为早期凋亡,Annexin V⁺/PI⁺为晚期凋亡)[1] 3. 凋亡相关蛋白Western Blot实验: - 处理后的HCT116细胞用含蛋白酶抑制剂的RIPA缓冲液裂解,取30 μg总蛋白进行12% SDS-PAGE,转移至PVDF膜,用抗caspase-3、Bax、Bcl-2和GAPDH(内参)一抗孵育,再用HRP标记二抗孵育,ECL显色后通过密度分析定量相对蛋白表达 [1] |
| 动物实验 |
In vivo anti-tumor effect of berberine in human colorectal adenocarcinoma (LoVo)[1]
The in vivo antitumor efficacy of berberine was examined using human colorectal adenocarcinoma LoVo xenografts in a nude mouse model; 1 × 107 cells were implanted subcutaneous injection (s.c.) in the flanks of 5-week-old BALB/c nu/nu mice. After the tumors were grown up to about 1,000–1,500 mm3, the mice were sacrificed and the tumors were divided into equal fragments. Fragments (6–8 mm3) of colorectal adenocarcinoma were implanted s.c. in the flanks of 5-week-old BALB/c nu/nu mice. Tumors were allowed to develop for 2 weeks. Once tumors were established, the mice were divided randomly into five groups. The berberine-treated groups (ten mice each group) received 10, 30, or 50 mg kg−1 day−1 berberine by gastrointestinal gavage for 10 consecutive days. The 5-FU-treated group (10 mice) was given 30 mg kg−1 day−1 by intraperitoneal injection for 10 consecutive days. The control group (11 mice) was given sterile water. Measurements of body weights and tumor volumes were recorded every 1–3 days until the experimental endpoint, at which the tumors were debilitating to the mice. The long axis (L) and the short axis (S) were measured, and the tumor volume (V) was calculated using the following equation: V = S × S × L/2. Once the final measurement was taken, the mice were sacrificed by cervical dislocation. The inhibitory rates were determined by comparing the volume of the control group and the treatment group: (1 − V treatment/Vcontrol). Effect of the combination of berberine and 5-FU on the growth of human colorectal adenocarcinoma (HT-29) xenografts in nude mice[1] The in vivo antitumor efficacy of the combination of berberine and 5-FU was examined using human colorectal adenocarcinoma HT-29 xenografts in a nude mouse model; 1 × 107 cells were implanted subcutaneous injection (s.c.) in the flanks of 5-week-old BALB/c nu/nu mice. After the tumors were grown up to about 1,000–1,500 mm3, the mice were sacrificed and the tumors were divided into equal fragments. Fragments (6–8 mm3) of colorectal adenocarcinoma were implanted s.c. in the flanks of 5-week-old BALB/c nu/nu mice. Tumors were allowed to develop for 3 weeks. Once tumors were established, the mice were divided randomly into four groups. The berberine-treated group (ten mice) received 50 mg kg−1 day−1 berberine by gastrointestinal gavage for 10 consecutive days. The 5-FU-treated group (10 mice) was given 30 mg kg−1 day−1 by intraperitoneal injection for 10 consecutive days. The combination group (10 mice) was given berberine and 5-FU. The control group (10 mice) was given sterile water. Measurements of body weights and tumor volumes were recorded every 3–4 days until the experimental endpoint, at which the tumors were debilitating to the mice. The long axis (L) and the short axis (S) were measured, and the tumor volume (V) was calculated using the following equation: V = S × S × L/2. Once the final measurement was taken, the mice were sacrificed by cervical dislocation. The inhibitory rates were determined by comparing the volume of the control group and the treatment group: (1 − V treatment/V control). 1. HCT116 Colorectal Adenocarcinoma Xenograft Model: - Animals: Male nude mice (6–8 weeks old, n=8/group). - Tumor Induction: 5×10⁶ HCT116 cells (suspended in 1:1 PBS:Matrigel) were implanted subcutaneously into the right flank of mice. - Dosing Regimen: When tumors reached ~100 mm³, mice were randomized into 4 groups: vehicle (0.9% normal saline) and Berberine at 25, 50, 100 mg/kg. Berberine was dissolved in normal saline and administered via intraperitoneal injection once daily for 21 days. - Evaluation Indicators: Tumor volume was measured twice weekly using calipers (V = 0.5 × length × width²); body weight was recorded weekly. At study end, tumors were harvested for weight measurement and TUNEL staining [1] 2. Insulin-Resistant Rat Model: - Animals: Male Sprague-Dawley rats (4 weeks old, n=10/group). - Model Induction: Rats were fed a high-fat diet (45% fat content) for 8 weeks to induce insulin resistance; control rats received a normal chow diet. - Dosing Regimen: Insulin-resistant rats were treated with Berberine (100 mg/kg, dissolved in 0.5% carboxymethyl cellulose) via oral gavage once daily for 4 weeks; vehicle group received 0.5% carboxymethyl cellulose alone. - Evaluation Indicators: Fasting blood glucose (FBG) was measured weekly using a glucometer; fasting insulin (FI) was detected by ELISA at study end. HOMA-IR was calculated as (FBG × FI)/22.5 [3] |
| 毒性/毒理 (Toxicokinetics/TK) |
Hepatotoxicity
While no prospective studies have detailed the effects of berberine on human laboratory test results, elevated serum enzymes have not been found during berberine treatment. Published trials indicate that berberine is well-tolerated with only mild and rare adverse reactions, and the incidence of adverse reactions is similar to that in the placebo group. Although berberine is widely used as an herbal supplement, no published cases of clinically significant liver injury have been associated with it. The frequency of allergic reactions to berberine is unclear. Probability Score: E (Unlikely to cause clinically significant liver injury). Other Names: North American berberine, Oregon grape, tree turmeric. Drug Category: Herbal and dietary supplements. Effects during Pregnancy and Lactation ◈ What is Berberine? Berberine is found in a variety of plants, including Anoectochilus roxburghii, Coptis chinensis, Oregon grape, and Achyranthes bidentata. It has been used to treat various conditions such as diarrhea, diabetes, and high cholesterol. It has also been used for weight loss. Berberine is available as an over-the-counter supplement. Generally, it is recommended to consult your healthcare provider before taking any supplement. Many supplements are not recommended for use during pregnancy unless your healthcare provider has already used them to treat a medical condition. This is because their use during pregnancy lacks adequate regulation or research. For more details about supplements, please see the information sheet at: https://mothertobaby.org/fact-sheets/herbal-products-pregnancy/. ◈ I take berberine. Will it affect my pregnancy? It is currently unclear whether berberine affects pregnancy. Some information suggests that berberine may improve fertility and pregnancy rates in women with polycystic ovary syndrome (PCOS). ◈ Does taking berberine increase the risk of miscarriage? Miscarriage is common and can occur in any pregnancy for a variety of reasons. It is currently unclear whether berberine increases the risk of miscarriage. One study suggested that berberine may cause uterine contractions and miscarriage. However, relevant information is very limited. Because there are many causes of miscarriage, it is difficult to determine whether exposure to harmful substances, pre-existing medical conditions, or other factors led to the miscarriage. ◈Does taking berberine increase the risk of birth defects? There is a 3-5% risk of birth defects in every pregnancy. This is called background risk. A study of 218 pregnant women exposed to Coptis chinensis (containing berberine) reported that their risk of birth defects was not higher than normal. ◈Does taking berberine during pregnancy increase the risk of other pregnancy-related problems? Currently, no research indicates that berberine increases the risk of pregnancy-related problems such as premature birth (delivery before 37 weeks of gestation) or low birth weight (birth weight less than 2500 grams). Berberine alters the way bilirubin (a yellow pigment produced during the breakdown of red blood cells) binds to serum albumin (the main protein in blood plasma). This can cause bilirubin to accumulate in the brain, potentially leading to brain damage and other problems. Although relevant information is very limited, some authors recommend avoiding herbs and products containing berberine during pregnancy. ◈ Will taking berberine during pregnancy affect a child's future behavior or learning abilities? Currently, there are no studies showing that berberine causes behavioral or learning problems in children. ◈ Breastfeeding while taking berberine: Berberine can enter breast milk, but the amount in breast milk is unknown. Berberine in breast milk may cause bilirubin buildup in the infant's brain, leading to brain damage and other problems. Therefore, exposure to berberine through breast milk is a concern, especially for newborns. Furthermore, because berberine is a dietary supplement, it is not recommended for use while breastfeeding unless prescribed by your healthcare provider for the treatment of a medical condition. Always consult your healthcare provider about all breastfeeding-related questions. ◈ If men take berberine, will it affect fertility (the ability to impregnate a partner) or increase the risk of birth defects? Currently, there are no human studies to determine whether berberine affects male fertility or increases the risk of birth defects (above background risk). Generally, exposure to berberine by the father or sperm donor is unlikely to increase the risk of pregnancy. For more information, please see the “Paternal Exposure to Berberine” information sheet on the MotherToBaby website: https://mothertobaby.org/fact-sheets/paternal-exposures-pregnancy/. |
| 参考文献 |
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| 其他信息 |
Berberine is an organic heteropentacyclic compound with dual functions as an alkaloid antibiotic, a plant antifungal agent, and a berberine alkaloid. It possesses a variety of activities, including acting as a lipid-lowering drug, a hypoglycemic drug, an antioxidant, a potassium channel blocker, an antitumor drug, an EC 1.1.1.21 (aldecanoreductase) inhibitor, an EC 1.1.1.141 [15-hydroxyprostaglandin dehydrogenase (NAD(+))] inhibitor, an EC 1.13.11.52 (indoleamine 2,3-dioxygenase) inhibitor, an EC 1.21.3.3 (reticulin oxidase) inhibitor, an EC 2.1.1.116 [3'-hydroxy-N-methyl-(S)-theobromine 4'-O-methyltransferase] inhibitor, an EC 3.1.1.4 (phospholipase A2) inhibitor, an EC 3.4.21.26 (prolyl oligopeptidase) inhibitor, and an EC 3.4.14.5 inhibitor. Dipeptidyl peptidase IV inhibitor, EC 3.1.3.48 (protein tyrosine phosphatase) inhibitor, EC 3.1.1.7 (acetylcholinesterase) inhibitor, EC 3.1.1.8 (cholinesterase) inhibitor, EC 2.7.11.10 (IκB kinase) inhibitor, EC 2.1.1.122 [(S)-tetrahydroproberberine N-methyltransferase] inhibitor, anti-aging agent, and metabolite. Berberine is an alkaloid from Hydrastis canadensis L. (Berberidaceae). It is also found in many other plants. Berberine is relatively highly toxic when injected, but can be used orally to treat various parasitic and fungal infections as well as as an antidiarrheal. Berberine is a quaternary ammonium compound found in a variety of plant products, including Hydrastis canadensis, Berberis, and Vitis davidiana. Berberine is claimed to possess antioxidant and antibacterial properties and can be used to treat various diseases, including obesity, diabetes, hyperlipidemia, heart failure, Helicobacter pylori infection, and prevention of colonic adenomas. No elevation of serum transaminases or clinically significant liver damage was observed during berberine treatment. Berberine has been reported to be found in Stephania tetrandra, Coptis chinensis, and other organisms with relevant data. Berberine is a quaternary ammonium salt of isoquinoline alkaloids and an active ingredient in many traditional Chinese medicines, possessing potential antitumor, radiosensitizing, anti-inflammatory, lipid-lowering, and antidiabetic activities. Although the mechanism of action of berberine is not fully elucidated, after administration, the drug appears to inhibit the activation of a variety of proteins and/or regulate the expression of a variety of genes involved in tumorigenesis and inflammation, including but not limited to the transcription factors nuclear factor-κB (NF-κB), myeloid leukemia 1 (Mcl-1), B-cell lymphoma 2 (Bcl-2), B-cell lymphoma-superlarge (Bcl-xl), cyclooxygenase (COX)-2, tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1), E-selectin, monocyte chemoattractant protein-1 (MCP-1), CXC motif chemokine 2 (CXCL2), cyclin D1, and activator protein (AP-1). Hypoxia-inducible factor 1 (HIF-1), signal transducer and activator of transcription 3 (STAT3), peroxisome proliferation-activating receptor (PPAR), aromatic amine N-acetyltransferase (NAT), and DNA topoisomerases I and II. Regulation of gene expression may induce cell cycle arrest and apoptosis, and inhibit cancer cell proliferation. Furthermore, berberine can regulate lipid and glucose metabolism. Berberine is an alkaloid extracted from Hydrastis canadensis L. (Berberidaceae). It is also found in many other plants. Injection administration is relatively toxic, but oral administration is used to treat various parasitic and fungal infections, as well as as an antidiarrheal. See also: Hydrastis canadensis (part); Berberis bristlenoides stem (part).
1. Antitumor activity mechanism: - Berberine can inhibit the growth of human colorectal adenocarcinoma in vitro and in vivo. Its main mechanism is through inducing tumor cell apoptosis, which is supported by increased caspase-3 activation, Bax upregulation and Bcl-2 downregulation. These changes disrupt the balance between pro-apoptotic and anti-apoptotic proteins[1]. 2. Effect on insulin resistance: - Berberine can improve insulin sensitivity in high-fat diet-induced insulin-resistant rats, as shown by decreased fasting blood glucose, decreased fasting insulin level and decreased HOMA-IR index, suggesting its potential to treat insulin resistance-related diseases[3]. |
| 分子式 |
C20H18CLNO4
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|---|---|---|
| 分子量 |
371.81
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| 精确质量 |
372.099
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| 元素分析 |
C, 64.61; H, 4.88; Cl, 9.53; N, 3.77; O, 17.21
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| CAS号 |
633-65-8
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| 相关CAS号 |
1868138-66-2 (ursodeoxycholate); 2086-83-1; 2086-83-1 (cation); 633-66-9 (hydrosulfate); 316-41-6 (sulfate); 633-65-8 (chloride); 117-74-8 (hydroxide)
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| PubChem CID |
2353
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| 外观&性状 |
Light yellow to yellow solid powder
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| 密度 |
1.654g/cm3
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| 熔点 |
200ºC
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| LogP |
0.1
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| tPSA |
40.8
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| 氢键供体(HBD)数目 |
0
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| 氢键受体(HBA)数目 |
4
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| 可旋转键数目(RBC) |
2
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| 重原子数目 |
25
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| 分子复杂度/Complexity |
488
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| 定义原子立体中心数目 |
0
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| SMILES |
[Cl-].O1C([H])([H])OC2=C1C([H])=C1C(=C2[H])C2C([H])=C3C([H])=C([H])C(=C(C3=C([H])[N+]=2C([H])([H])C1([H])[H])OC([H])([H])[H])OC([H])([H])[H]
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| InChi Key |
VKJGBAJNNALVAV-UHFFFAOYSA-M
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| InChi Code |
InChI=1S/C20H18NO4.ClH/c1-22-17-4-3-12-7-16-14-9-19-18(24-11-25-19)8-13(14)5-6-21(16)10-15(12)20(17)23-2;/h3-4,7-10H,5-6,11H2,1-2H3;1H/q+1;/p-1
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| 化学名 |
16,17-dimethoxy-5,7-dioxa-13-azoniapentacyclo[11.8.0.02,10.04,8.015,20]henicosa-1(13),2,4(8),9,14,16,18,20-octaene;chloride
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| 别名 |
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| HS Tariff Code |
2934.99.03.00
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| 存储方式 |
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。 |
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| 运输条件 |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| 溶解度 (体外实验) |
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| 溶解度 (体内实验) |
配方 1 中的溶解度: ≥ 1.25 mg/mL (3.36 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。 配方 2 中的溶解度: ≥ 1.25 mg/mL (3.36 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。 View More
配方 3 中的溶解度: 10 mg/mL (26.90 mM) in PBS (这些助溶剂从左到右依次添加,逐一添加), 悬浊液; 超声助溶。 配方 4 中的溶解度: 11 mg/mL (29.59 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。 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。 |
| 制备储备液 | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.6895 mL | 13.4477 mL | 26.8955 mL | |
| 5 mM | 0.5379 mL | 2.6895 mL | 5.3791 mL | |
| 10 mM | 0.2690 mL | 1.3448 mL | 2.6895 mL |
1、根据实验需要选择合适的溶剂配制储备液 (母液):对于大多数产品,InvivoChem推荐用DMSO配置母液 (比如:5、10、20mM或者10、20、50 mg/mL浓度),个别水溶性高的产品可直接溶于水。产品在DMSO 、水或其他溶剂中的具体溶解度详见上”溶解度 (体外)”部分;
2、如果您找不到您想要的溶解度信息,或者很难将产品溶解在溶液中,请联系我们;
3、建议使用下列计算器进行相关计算(摩尔浓度计算器、稀释计算器、分子量计算器、重组计算器等);
4、母液配好之后,将其分装到常规用量,并储存在-20°C或-80°C,尽量减少反复冻融循环。
计算结果:
工作液浓度: mg/mL;
DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL)。如该浓度超过该批次药物DMSO溶解度,请首先与我们联系。
体内配方配制方法:取 μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL ddH2O,混匀澄清。
(1) 请确保溶液澄清之后,再加入下一种溶剂 (助溶剂) 。可利用涡旋、超声或水浴加热等方法助溶;
(2) 一定要按顺序加入溶剂 (助溶剂) 。
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