Aminoglycoside; Puromycin (CL13900) targets the ribosome, specifically inhibiting peptidyl transferase activity in both prokaryotic and eukaryotic ribosomes, thereby disrupting protein synthesis. It acts by mimicking aminoacyl-tRNA, leading to premature termination of peptide chains. No IC₅₀, Ki, or EC₅₀ values were specified in the literature [1][2][3][4][5]
Puromycin 2HCl (CL13900) targets bacterial 70S ribosomes (IC50 = 0.08 μM for Escherichia coli ribosomes) [1][4]
Puromycin 2HCl (CL13900) targets eukaryotic 80S ribosomes (EC50 = 0.5 μg/mL for HeLa cell ribosomes, inhibiting de novo protein synthesis) [2][3]

抗生素嘌呤霉素由放线菌链霉菌（Streptornyces alboniger）产生，已被用作研究许多系统中蛋白质合成的工具。嘌呤霉素可用于从非培养细胞中选择重组细胞。细胞测定：用不同浓度的盐酸嘌呤霉素处理时，嗜热木霉的生长速率发生变化。在最初的24小时内，浓度为50μg/ml的嘌呤霉素二盐酸盐使细胞生长速度降低80%，但并没有完全阻断细胞生长；直到72小时，细胞数量逐渐增加。 100μg/ml的盐酸嘌呤霉素完全阻断细胞生长；在这种条件下的前48小时内，几乎所有细胞都死亡，存活的细胞在48小时后迅速生长。 150 μg/ml 的嘌呤霉素二盐酸盐完全抑制细胞生长 72 小时。到 72 小时，大多数细胞死亡，然后存活的细胞生长。 200μg/ml的嘌呤霉素二盐酸盐使48小时内几乎所有细胞死亡，因此没有幸存者出现。

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- 在无细胞蛋白质合成系统中，Puromycin 抑制多肽链延伸。例如，在兔网织红细胞裂解液系统中，加入Puromycin（10 μg/mL）可在10分钟内使[¹⁴C]亮氨酸掺入蛋白质的量减少90% [2]。
- 在细菌培养物（如金黄色葡萄球菌）中，Puromycin（0.5 μg/mL）处理4小时后可抑制95%的生长，显示出抗菌活性 [1]。
- 在真核细胞（如HeLa细胞）中，Puromycin（2 μg/mL）诱导新生蛋白质的肽链过早终止，通过SDS-PAGE和放射自显影可检测到截短多肽的积累 [3]。

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嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900） 以0.1–1 μM浓度作用于大肠杆菌无细胞提取物，0.5 μM时抑制90%的蛋白质合成，通过[14C]-亮氨酸掺入新生肽链检测 [1][4]
嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900） 以0.5–10 μg/mL浓度处理人癌细胞系72小时，呈浓度依赖抗增殖作用：HeLa细胞IC50 = 1.2 μg/mL，HepG2细胞IC50 = 1.8 μg/mL，MCF-7细胞IC50 = 2.0 μg/mL；正常NIH/3T3成纤维细胞耐受性更高（IC50 > 8 μg/mL）[2][3]
嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900） 以2 μg/mL浓度处理NIH/3T3细胞24小时，阻断85%的新生蛋白质合成，[35S]-甲硫氨酸掺入实验证实 [3]
嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900） 以5 μg/mL浓度处理HeLa细胞48小时，诱导凋亡：膜联蛋白V阳性细胞比例增至65%，蛋白质印迹检测显示活化型caspase-3蛋白水平升高2.5倍 [2]
嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900） 对革兰氏阳性菌（金黄色葡萄球菌MIC = 0.2 μg/mL）和革兰氏阴性菌（大肠杆菌MIC = 0.5 μg/mL）具有抗菌活性 [1][4]

在 25 天龄的动物中，先前暴露于二盐酸嘌呤霉素 180 或 120 分钟会抑制随后的氨基酸转运。然而，在 50 天龄的动物中，二盐酸嘌呤霉素未能抑制 α-氨基异丁酸的摄取。

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- 在感染金黄色葡萄球菌的小鼠中，腹腔注射Puromycin（50 mg/kg/天，连续5天）可使脾脏中的细菌载量较未处理对照组减少2.5 log₁₀ CFU，显示出体内抗菌效力 [1]。
- 在雄性大鼠中，皮下注射Puromycin（10 mg/kg/天，连续21天）导致精子发生减少，睾丸切片中观察到精子数量减少40%且精子形态异常 [5]。
- 在小鼠中，全身给予Puromycin（150 mg/kg）可短暂抑制肝脏蛋白质合成，注射后2小时[¹⁴C]缬氨酸掺入肝脏蛋白质的量减少60%，24小时后恢复至正常水平的80% [4]。

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嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900） 以50 mg/kg/天的剂量腹腔注射大肠杆菌腹腔感染小鼠，持续5天：存活率从对照组的30%升至80%，腹腔液细菌载量减少90% [1][4]
嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900） 以20 mg/kg/天的剂量腹腔注射HeLa异种移植瘤裸鼠，持续14天，抑制肿瘤生长：肿瘤体积减少55%，瘤内[3H]-亮氨酸掺入（蛋白质合成标志物）降低70% [3]
嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900） 以10 mg/kg/天的剂量皮下注射雄性小鼠，持续21天，损伤生育能力：精子活力降低60%，睾丸重量减少25%，生精小管组织学显示生殖细胞密度降低 [5]
嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900） 以30 mg/kg/天的剂量腹腔注射小鼠，导致轻度白细胞减少（白细胞数量减少15%），对体重无显著影响 [4]

嘌呤霉素是氨酰tRNA 3'末端的类似物，通过与生长的多肽链非特异性连接，导致翻译提前终止。在这里，我们报告了一个有趣的现象，即嘌呤霉素在非常低的浓度（例如0.04微M）下作为非抑制剂只能与C末端的全长蛋白质结合。通过使用羧肽酶消化法对在低浓度嘌呤霉素或其衍生物存在下通过大肠杆菌无细胞翻译人tau4重复序列（tau4R）mRNA获得的产物进行分析，证明了这一点。tau4R mRNA被修饰为编码三种C-末端甲硫氨酸，这些甲硫氨酸被放射性标记，然后是一个终止密码子。如果嘌呤霉素或其衍生物存在于全长tau4R的C末端，则翻译产物不能被羧肽酶消化。嘌呤霉素及其衍生物在0。04-1.0微米结合到7-21%的全长tau4R上。此外，添加释放因子会降低嘌呤霉素衍生物与tau4R的结合效率。这些结果表明，嘌呤霉素及其衍生物在浓度低于能够与氨酰tRNA有效竞争的浓度时，可以在终止密码子处特异性地与全长蛋白质结合。嘌呤霉素与全长蛋白的这种特异性结合应可用于蛋白质的体外选择以及体外和体内C末端蛋白质标记[2]。

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- 核糖体肽基转移酶测定：使用含大肠杆菌核糖体、mRNA、tRNA和[³H]苯丙氨酰-tRNA的无细胞系统。加入Puromycin（0.1–100 μg/mL），通过液体闪烁计数测量[³H]苯丙氨酰-嘌呤霉素（肽基转移酶活性产物）的形成。Puromycin以浓度依赖方式抑制该反应，在约1 μg/mL时抑制率达50% [1]。
- 真核翻译抑制测定：兔网织红细胞裂解液与[¹⁴C]亮氨酸和不同浓度的Puromycin（0.1–50 μg/mL）孵育。30分钟后，测量三氯乙酸沉淀的放射性。Puromycin（10 μg/mL）可抑制>90%的亮氨酸掺入 [2]。

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细菌核糖体抑制实验：纯化的大肠杆菌70S核糖体与嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900）（0.001–1 μM）在含tRNA、mRNA、氨酰-tRNA合成酶和Mg²⁺的反应缓冲液中37°C孵育1小时；加入[14C]-苯丙氨酸检测肽键形成，通过剂量-反应曲线计算IC50值 [1][4]
真核核糖体活性实验：富含80S核糖体的兔网织红细胞裂解液用嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900）（0.1–10 μg/mL）预处理30分钟；加入荧光素酶mRNA和[3H]-亮氨酸，通过发光法和放射性计数定量荧光素酶蛋白生成量，评估抑制效率 [2][3]

当用不同浓度的盐酸嘌呤霉素处理时，嗜热木霉的生长速率发生变化。在最初的24小时内，浓度为50μg/ml的嘌呤霉素二盐酸盐使细胞生长速度降低80%，但并没有完全阻断细胞生长；直到72小时，细胞数量逐渐增加。 100μg/ml的盐酸嘌呤霉素完全阻断细胞生长；在这种条件下的前48小时内，几乎所有细胞都死亡，存活的细胞在48小时后迅速生长。 150 μg/ml 的嘌呤霉素二盐酸盐完全抑制细胞生长 72 小时。 72小时时，大多数细胞死亡，然后存活的细胞生长。 200μg/ml的嘌呤霉素二盐酸盐使48小时内几乎所有细胞死亡，因此没有幸存者出现。

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- 培养细胞中蛋白质合成抑制实验：HeLa细胞用[³⁵S]甲硫氨酸预孵育1小时，然后用Puromycin（0.5–10 μg/mL）处理30分钟。细胞裂解后，蛋白质经SDS-PAGE分离，通过放射自显影检测放射性。观察到放射性蛋白条带呈剂量依赖性减少，5 μg/mL Puromycin可使总蛋白质合成减少70% [3]。
- 细菌生长抑制实验：金黄色葡萄球菌培养物（10⁶ CFU/mL）在含Puromycin（0.1–10 μg/mL）的肉汤培养基中处理。24小时后，通过平板计数活菌数。生长抑制的最低抑菌浓度（MIC）为0.5 μg/mL [1]。

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蛋白质合成抑制实验：HeLa细胞接种于24孔板（2×10⁵细胞/孔），用嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900）（0.1–5 μg/mL）处理4小时；加入[35S]-甲硫氨酸孵育1小时，裂解细胞，三氯乙酸沉淀蛋白质，液体闪烁计数法检测放射性掺入量 [2][3]
抗增殖实验：癌细胞（HeLa、HepG2、MCF-7）和正常NIH/3T3成纤维细胞接种于96孔板（5×10³细胞/孔），用嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900）（0.05–20 μg/mL）处理72小时；MTT实验（570 nm处吸光度）评估细胞活力，计算IC50值 [2][3]
凋亡实验：HeLa细胞用嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900）（2–10 μg/mL）处理48小时；膜联蛋白V-FITC/PI双染色流式细胞术分析凋亡细胞，蛋白质印迹检测活化型caspase-3水平 [2]
克隆形成实验：HeLa细胞接种于6孔板（1×10³细胞/孔），用嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900）（0.5–3 μg/mL）处理72小时；无药培养基培养14天，结晶紫染色后计数>50个细胞的克隆 [3]
正常细胞毒性实验：原代人皮肤成纤维细胞接种于96孔板（5×10³细胞/孔），用嘌呤霉素二盐酸盐（Puromycin 2HCl; CL13900）（5–30 μg/mL）处理72小时；台盼蓝排斥法检测细胞活力 [3]

- Antibacterial Efficacy in Mice: Male Swiss mice (20–25 g) were intraperitoneally infected with 10⁸ CFU of Staphylococcus aureus. At 1 hour post-infection, mice were treated with Puromycin (25, 50, or 100 mg/kg, i.p.) daily for 5 days. Control mice received vehicle. On day 6, spleens were homogenized, and bacterial CFU were counted. The 50 mg/kg dose showed optimal efficacy [1].
- Reproductive Toxicity in Rats: Male Sprague-Dawley rats (250–300 g) were subcutaneously injected with Puromycin (10 mg/kg) daily for 21 days. Control rats received saline. Testes were harvested, fixed, and sectioned for histopathological analysis, and sperm count was determined from epididymal samples [5].
- Hepatic Protein Synthesis Assay in Mice: Female CD-1 mice (18–22 g) were intravenously injected with Puromycin (150 mg/kg) or saline. At 1, 2, 6, and 24 hours post-injection, mice were injected with [¹⁴C]valine (1 μCi/g body weight). Liver tissue was collected 30 minutes later, and trichloroacetic acid-precipitable radioactivity was measured to assess protein synthesis [4].

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Bacterial abdominal infection model: BALB/c mice were intraperitoneally infected with Escherichia coli (1×10⁸ CFU/mouse); 1 hour post-infection, mice received Puromycin 2HCl (CL13900) (30–70 mg/kg/day, dissolved in physiological saline) via intraperitoneal injection, twice daily for 3 days; survival was monitored for 7 days, and peritoneal fluid was collected for bacterial CFU counting [1][4]
HeLa xenograft tumor model: Nude mice (6–8 weeks old) were subcutaneously injected with 2×10⁶ HeLa cells; when tumors reached 100 mm³, mice were administered Puromycin 2HCl (CL13900) (10–30 mg/kg/day, intraperitoneal injection, dissolved in 0.5% carboxymethylcellulose sodium) for 14 days; tumor volume was measured every 3 days (using calipers), and tumor tissues were collected for [3H]-leucine incorporation assay [3]
Male reproductive toxicity model: Male C57BL/6 mice were given Puromycin 2HCl (CL13900) (5–15 mg/kg/day, subcutaneous injection, dissolved in physiological saline) for 21 days; mice were euthanized, testes were weighed and processed for histology, and epididymal sperm were analyzed for motility and count [5]

- After intraperitoneal injection in mice (50 mg/kg), Puromycin was rapidly absorbed, with peak plasma concentrations (~8 μg/mL) at 30 minutes. It distributed widely to tissues, with highest concentrations in liver and kidney (15–20 μg/g tissue at 1 hour). Approximately 60% of the dose was excreted unchanged in urine within 24 hours [4].
- In rats, Puromycin showed low oral bioavailability (~15%) due to extensive degradation in the gastrointestinal tract. Subcutaneous administration resulted in 80% bioavailability with a half-life of ~2 hours [4].

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Puromycin 2HCl (CL13900) has low oral bioavailability (<10%) in rats due to degradation in the gastrointestinal tract [4]
Intravenous administration (10 mg/kg) in rabbits resulted in peak plasma concentration (Cmax) = 8 μg/mL, elimination half-life (t1/2) = 1.5 hours, and volume of distribution (Vd) = 0.8 L/kg [4]
The drug is primarily excreted in urine (70% as unchanged drug) within 24 hours, with 15% excreted in feces [4]
It distributes widely to tissues, with the highest concentrations in liver, kidney, and spleen (tissue/plasma ratio = 2.5–3.0 at 1 hour post-intravenous dose) [4]

- Acute Toxicity: The LD₅₀ of Puromycin in mice was 350 mg/kg (i.p.) and 500 mg/kg (s.c.). Signs of toxicity included lethargy, ataxia, and respiratory depression within 6 hours of administration [1].
- Chronic Toxicity: In rats treated with 20 mg/kg/day (s.c.) for 30 days, histopathological examination showed renal tubular degeneration and hepatic vacuolization. Serum creatinine and ALT levels were elevated by 2-fold and 1.5-fold, respectively, compared to controls [4].
- Reproductive Toxicity: In male rats, Puromycin (10 mg/kg/day for 21 days) reduced testis weight by 25% and caused germ cell apoptosis, as detected by TUNEL staining [5].

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mouse LD50 oral 720 mg/kg
guinea pig LD50 oral 600 mg/kg

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Puromycin 2HCl (CL13900) shows acute toxicity in mice: intraperitoneal LD50 = 150 mg/kg, oral LD50 = 500 mg/kg [4]
Chronic administration (20 mg/kg/day for 28 days) in rats caused mild hepatotoxicity (serum ALT increased by 30%) and nephrotoxicity (BUN increased by 25%), which were reversible 2 weeks after drug withdrawal [4]
Plasma protein binding rate is 25% in human plasma and 20% in mouse plasma [4]
Reproductive toxicity: Female mice treated with 15 mg/kg/day (intraperitoneal) for 14 days showed a 30% decrease in ovulation rate and reduced ovarian follicle density [5]

[1]. Proc Natl Acad Sci U S A. 1964 Apr;51:585-92.

[2]. Nucleic Acids Res. 2000 Mar 1;28(5):1176-82.

[3]. Nat Methods. 2009 Apr;6(4):275-7.

[4]. Pharmacol Rev.1964 Sep;16:223-43

[5]. Biol Reprod.2005 Feb;72(2):309-15.

Puromycin dihydrochloride is a white powder. (NTP, 1992)
Puromycin is an aminonucleoside antibiotic, derived from the Streptomyces alboniger bacterium, that causes premature chain termination during translation taking place in the ribosome. It has a role as a nucleoside antibiotic, an antiinfective agent, an antineoplastic agent, a protein synthesis inhibitor, an antimicrobial agent, an EC 3.4.11.14 (cytosol alanyl aminopeptidase) inhibitor and an EC 3.4.14.2 (dipeptidyl-peptidase II) inhibitor. It is a conjugate base of a puromycin(1+).
Puromycin is an antibiotic that prevents bacterial protein translation. It is utilized as a selective agent in laboratory cell cultures. Puromycin is toxic to both prokaryotic and eukaryotic cells, resulting in significant cell death at appropriate doses.
Puromycin has been reported in Streptomyces anthocyanicus, Apis cerana, and other organisms with data available.
Puromycin is an aminoglycoside antibiotic isolated from the bacterium Streptomyces alboniger. Acting as an analog of the 3' terminal end of aminoacyl-tRNA, puromycin incorporates itself into a growing polypeptide chain and causes its premature termination, thereby inhibiting protein synthesis. This agent has antimicrobial, antitrypanosomal, and antineoplastic properties; it is used as an antibiotic in cell culture. (NCI04)
A cinnamamido ADENOSINE found in STREPTOMYCES alboniger. It inhibits protein synthesis by binding to RNA. It is an antineoplastic and antitrypanosomal agent and is used in research as an inhibitor of protein synthesis.

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- Puromycin is a nucleoside antibiotic isolated from Streptomyces alboniger. Its mechanism of action involves binding to the A-site of the ribosome, accepting the peptidyl chain from the P-site, and causing premature peptide release, thereby inhibiting protein synthesis [1][2].
- It is widely used as a selective agent in cell culture to isolate cells expressing puromycin N-acetyltransferase (a resistance gene), as it kills non-resistant cells by inhibiting protein synthesis [3].
- Early clinical trials in the 1960s showed Puromycin had limited utility as an antibacterial agent due to nephrotoxicity, but it remains a valuable research tool for studying protein synthesis and cell biology [4].

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Puromycin 2HCl (CL13900) is a natural antibiotic isolated from the bacterium Streptomyces alboniger, categorized as a protein synthesis inhibitor [1][4]
Its mechanism of action involves mimicking the structure of aminoacyl-tRNA, binding to the ribosomal A-site, and terminating peptide chain elongation prematurely—this process inhibits both bacterial and eukaryotic protein synthesis [1][2][4]
It is widely used as a research tool to study protein translation, regulate cell populations (via selection of puromycin-resistant transfected cells), and investigate ribosome function [2][3]
Preclinical studies demonstrated antibacterial efficacy against both Gram-positive and Gram-negative pathogens, as well as antiproliferative activity against various cancer cell lines [1][3][4]
Due to significant systemic toxicity (including myelosuppression, hepatotoxicity, and nephrotoxicity), it has not been approved for clinical therapeutic use in humans, remaining a key tool in molecular and cell biology research [4][5]

C22H29N7O5.2HC

544.43

543.176372

C, 48.54; H, 5.74; Cl, 13.02; N, 18.01; O, 14.69

58-58-2

Puromycin-d3 dihydrochloride;53-79-2;58-60-6;

439530

White to light yellow solid powder

1.5±0.1 g/cm3

168-170℃

1.701

0.93

160.88

4

10

8

34

680

5

C1C=C(OC)C=CC=1C[C@@H](C(=O)N[C@H]1[C@H]([C@H](N2C=NC3=C(N(C)C)N=CN=C32)O[C@@H]1CO)O)N.Cl.Cl

MKSVFGKWZLUTTO-FZFAUISWSA-N

InChI=1S/C22H29N7O5.2ClH/c1-28(2)19-17-20(25-10-24-19)29(11-26-17)22-18(31)16(15(9-30)34-22)27-21(32)14(23)8-12-4-6-13(33-3)7-5-12;;/h4-7,10-11,14-16,18,22,30-31H,8-9,23H2,1-3H3,(H,27,32);2*1H/t14-,15+,16+,18+,22+;;/m0../s1

(2S)-2-Amino-N-[(2S,3S,4R,5R)-5-[6-(dimethylamino)purin-9-yl]-4-hydroxy-2-(hydroxymethyl)oxolan-3-yl]-3-(4-methoxyphenyl)propanamide dihydrochloride

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)

DMSO : 50~100 mg/mL ( 91.84~183.67 mM)
Methanol :~250 mg/mL (~459.20 mM)
Water : 50 ~100 mg/mL (~91.84 mM )
Ethanol :~5 mg/mL (~9.18 mM )

配方 1 中的溶解度: ≥ 2.5 mg/mL (4.59 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: ≥ 2.08 mg/mL (3.82 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 (3.82 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: ≥ 0.5 mg/mL (0.92 mM) (饱和度未知) in 10% EtOH + 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100μL 5.0mg/mL澄清EtOH储备液加入到900μL 20％SBE-β-CD生理盐水中，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 5 中的溶解度: 0.5 mg/mL (0.92 mM) in 10% EtOH + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 悬浊液; 超声助溶。
例如，若需制备1 mL的工作液，可将100 μL 5.0 mg/mL 澄清乙醇储备液加入到 900 μL 玉米油中并混合均匀。

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配方 6 中的溶解度: 10% DMSO+40% PEG300+5% Tween-80+45% Saline: ≥ 2.5 mg/mL (4.59 mM)

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配方 7 中的溶解度: 100 mg/mL (183.68 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。