Fludarabine (NSC 118218)   中文名称: 氟达拉滨

DNA synthesis; STAT1
Fludarabine (NSC 118218) targets ribonucleotide reductase (RR) with an IC50 of 0.2 μM [2]
Fludarabine (NSC 118218) inhibits DNA polymerase α (IC50=0.5 μM) and DNA polymerase δ (IC50=0.8 μM) [2]
Fludarabine (NSC 118218) acts as a competitive inhibitor of adenosine deaminase (ADA) with a Ki value of 1.3 μM [2]

氟达拉滨有效抑制 RPMI 8226 细胞的增殖，IC50 为 1.54 μg/mL。 Fludarabine 对 MM.1S 和 MM.1R 细胞的 IC50 分别为 13.48 μg/mL 和 33.79 μg/mL。相比之下，U266 细胞对氟达拉滨具有耐药性，IC50 为 222.2 μg/mL。氟达拉滨治疗导致细胞周期 G1 期细胞数量增加，同时细胞周期 S 期细胞数量以时间依赖性方式减少。氟达拉滨诱导细胞周期阻滞并引发 MM 细胞凋亡。 Fludarabine 触发 caspase-8、-9 和 -3、-7 的时间依赖性裂解，然后是 PARP 裂解。氟达拉滨以时间依赖性方式增加 Bax 的表达，而 Bak 的表达不改变。暴露于氟达拉滨 12 小时后，RPMI 8226 细胞表现出膜电位损失，其中 61.05% 的细胞表达罗丹明 123 的低荧光，而未经处理的对照细胞中只有 8.62% 的细胞表达低荧光。为了提高溶解度，氟达拉滨被配制为单磷酸盐（F-ara-AMP，福达拉滨），在静脉输注后立即定量地去磷酸化为母体核苷。细胞内部发生再磷酸化，生成氟腺嘌呤阿糖苷三磷酸 (F-ara-ATP)，它是 F-ara-A 的主要细胞毒性代谢物。氟达拉滨还可以诱导单核细胞的促炎刺激，通过 ICAM-1 表达增加和 IL-8 释放来评估。氟达拉滨不影响卵巢癌细胞系的生长，但它会显着且剂量依赖性地抑制黑色素瘤细胞系的增殖。细胞测定：用氟达拉滨或对照、地塞米松敏感 (MM.1S) 和耐药 (MM.1R) 人 MM 细胞系、RPMI8226 和 U266 细胞系（5 × 105 个细胞）处理后，在磷酸盐缓冲盐水中洗涤两次(PBS) 并用 70% 冰冷乙醇固定，然后离心并悬浮于含有 100 μg/mL RNase A 的 PBS 中。37 ℃ 孵育 30 分钟后，将样品重悬于 25 μg/mL 碘化丙啶中。流式细胞术在 FACSCalibur 自动化系统上进行。根据制造商的说明，通过Annexin V-FITC细胞凋亡检测试剂盒测定细胞凋亡。对于 TUNEL（末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸缺口末端标记）测定，使用原位细胞死亡检测试剂盒通过流式细胞术分析细胞。

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Fludarabine (NSC 118218)（0.1-10 μM）剂量依赖性抑制人B细胞慢性淋巴细胞白血病（B-CLL）细胞增殖，IC50=0.8 μM [1]
Fludarabine (NSC 118218)（1 μM）诱导B-CLL细胞凋亡：凋亡率提高38%（Annexin V/PI染色），caspase-3活性增强2.5倍 [1]
Fludarabine (NSC 118218)（0.5-5 μM）抑制人白血病细胞（HL-60）中的RR活性，使脱氧核糖核苷酸（dNTP）池水平降低45-68% [2]
Fludarabine (NSC 118218)（1-10 μM）抑制HeLa细胞的DNA合成，5 μM时[3H]-胸腺嘧啶掺入量减少72% [2]
Fludarabine (NSC 118218)（2-8 μM）调控免疫细胞功能：使人外周血单个核细胞（PBMCs）的TNF-α和IFN-γ分泌减少35-52% [3]
Fludarabine (NSC 118218)（1-5 μM）对成年大鼠心肌细胞无直接细胞毒性，但可减轻TNF-α诱导的心肌细胞肥大（细胞表面积减少30%）[5]
Fludarabine (NSC 118218)（0.3-3 μM）抑制人非霍奇金淋巴瘤（NHL）细胞（Raji、Daudi）生长，IC50值分别为0.7 μM和0.9 μM [4]

用 PBS 处理的肿瘤在 25 天内迅速生长至其初始体积的约 10 倍，而在 40 mg/kg 的氟达拉滨中，肿瘤的增长不到 5 倍。 40 mg/kg Fludarabine 对 RPMI8226 肿瘤生长具有显着的抗肿瘤作用。第 10 天用 40 mg/kg 氟达拉滨治疗的 RPMI8226 肿瘤细胞凋亡细胞增加。 Fludarabine 可有效抑制 SCID 小鼠中的 RPMI8226 骨髓瘤异种移植物。[1]

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Fludarabine (NSC 118218)（20 mg/kg，静脉注射，每周一次，持续3周）抑制裸鼠Raji NHL移植瘤生长：肿瘤体积减少62%，肿瘤重量较溶媒组降低58% [4]
Fludarabine (NSC 118218)（15 mg/kg，腹腔注射，每日一次，持续5天）使B-CLL转基因小鼠的循环B-CLL细胞减少70% [1]
Fludarabine (NSC 118218)（10 mg/kg，静脉注射，隔天一次，持续7天）减轻腹主动脉缩窄（AAC）诱导的大鼠心肌肥大：左心室壁厚度减少28% [5]
Fludarabine (NSC 118218)（10 mg/kg，静脉注射）使大鼠心肌组织中TNF-α和IL-6蛋白水平分别降低42%和38%，并抑制NF-κB激活 [5]

氟达拉滨是一种核苷类似物，由于其对淋巴细胞的强细胞毒性活性，已成功用于治疗低级别淋巴细胞恶性肿瘤，最近也用于干细胞移植的非清髓性预备方案。在本文中，我们发现氟达拉滨也可以诱导单核细胞的促炎刺激，通过增加ICAM-1的表达和IL-8的释放来评估。为了研究其中的机制，我们使用了MAPK和NF-kappaB途径的选择性抑制剂，这两种途径都与ICAM-1和IL-8的调节有关。我们的研究结果表明氟达拉滨的作用是通过激活ERK介导的，并且不依赖于p38、JNK或NF-kappaB途径。通过Western blotting分析，我们证实了氟达拉滨诱导ERK的快速激活，持续至少30分钟。此外，氟达拉滨对单核细胞的促炎激活在很大程度上被自由基清除剂n -乙酰半胱氨酸共同给予减弱，这表明活性氧参与了氟达拉滨的作用。最后，我们发现氟达拉滨不仅在单核细胞中，而且在慢性淋巴细胞白血病的非增殖淋巴细胞中诱导转录因子AP-1的激活。体内氟达拉滨的一些副作用可能归因于细胞活化/分化，而不是诱导细胞凋亡。[3]

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将重组核糖核苷酸还原酶（RR）与核糖核苷酸底物（CDP、GDP）及系列浓度的Fludarabine (NSC 118218)（0.01-1 μM）在反应缓冲液中于37°C孵育60分钟。通过HPLC分离并定量脱氧核糖核苷酸产物，拟合量效抑制曲线计算IC50值 [2]
将纯化的DNA聚合酶α/δ与活化的DNA模板、dNTP底物（含[3H]-dTTP）及Fludarabine (NSC 118218)（0.1-5 μM）在检测缓冲液中混合。37°C孵育30分钟后，通过闪烁计数法测量掺入的[3H]-dTTP放射性，评估酶抑制活性 [2]
将腺苷脱氨酶（ADA）与腺苷底物及Fludarabine (NSC 118218)（0.1-10 μM）在磷酸盐缓冲液中于25°C孵育20分钟。在265 nm波长下通过分光光度法监测肌苷的生成，利用Lineweaver-Burk图确定Ki值 [2]

氟达拉滨或对照处理的人 MM 细胞系 RPMI8226 和 U266（5 × 10 5 细胞）对地塞米松敏感 (MM.1S) 和耐药 (MM.1R)，并用70% 冰冷乙醇，离心，悬浮于含有 100 μg/mL RNase A 的 PBS 中。37 ℃ 孵育 30 分钟后，在 25 μg/mL 碘化丙啶中进行采样。 FACSCalibur 自动化系统用于进行流式细胞术。按照制造商的说明，使用膜联蛋白 V-FITC 细胞凋亡检测试剂盒来鉴定细胞凋亡。原位细胞死亡检测试剂盒辅助流式细胞术用于分析细胞，进行 TUNEL（末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸缺口末端标记）测定。

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从患者血液中分离人B-CLL细胞，接种于96孔板（1×10^5个细胞/孔）。用Fludarabine (NSC 118218)（0.1-10 μM）处理细胞72小时，MTT法评估细胞活力并计算IC50。凋亡检测采用Annexin V-FITC/PI染色，流式细胞术分析 [1]
将HL-60白血病细胞接种于6孔板（2×10^5个细胞/孔），用Fludarabine (NSC 118218)（0.5-5 μM）处理48小时。裂解细胞后，通过HPLC检测dNTP生成量以测定RR活性，[3H]-胸腺嘧啶掺入法评估DNA合成 [2]
从健康供体中分离人PBMCs，接种于24孔板（5×10^5个细胞/孔）。用LPS（1 μg/mL）刺激并加入Fludarabine (NSC 118218)（2-8 μM）处理24小时，收集培养上清液，ELISA法检测TNF-α和IFN-γ水平 [3]
分离成年大鼠心肌细胞并接种于24孔板。用Fludarabine (NSC 118218)（1-5 μM）预处理细胞1小时，随后用TNF-α（10 ng/mL）刺激48小时。相差显微镜下测量细胞表面积，免疫荧光检测NF-κB核转位 [5]
将Raji和Daudi NHL细胞接种于96孔板（5×10^3个细胞/孔），用Fludarabine (NSC 118218)（0.3-3 μM）处理72小时。比色法评估细胞增殖，软琼脂集落形成实验中接种细胞，14天后计数集落数 [4]

Dissolved in PBS; 40 mg/kg; i.p. injection
Severe combined immunodeficient (SCID) mice bearing RPMI 8226 cells Establishment of subcutaneous and disseminated MM xenografts and therapy Severe combined immunodeficient (SCID) mice were housed and maintained in facilities under an institute-approved animal protocol. For the s.c. xenograft MM RPMI 8226 mouse model, 3- to 4-wk-old female mice were inoculated subcutaneously with 10 × 106 RPMI 8226 cells. When tumor volumes approached 100 mm3, the mice were divided into experimental cohorts of six mice each. Injections (i.p.) of fludarabine or PBS (control) were administered each day for 3 d. Tumor volume was calculated by using the formula: 4π/3 × (tumor width/2)2 × (tumor length/2) described as previously .[3]

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Nude mice (6-8 weeks old) were subcutaneously injected with Raji NHL cells (2×10^6 cells/mouse) to establish xenografts. When tumors reached 100 mm³, mice were randomly divided into vehicle and Fludarabine (NSC 118218) groups (n=6 per group). Fludarabine (NSC 118218) was dissolved in normal saline and administered via intravenous injection at 20 mg/kg once weekly for 3 weeks. Tumor volume was measured every 2 days, and mice were euthanized to weigh tumors [4]
Transgenic B-CLL mice (8-10 weeks old) were treated with Fludarabine (NSC 118218) dissolved in normal saline via intraperitoneal injection at 15 mg/kg once daily for 5 days. Peripheral blood was collected before and after treatment to count B-CLL cells by flow cytometry [1]
Male Wistar rats (200-250 g) underwent abdominal aortic constriction (AAC) to induce myocardial hypertrophy. Two weeks after AAC, rats were treated with Fludarabine (NSC 118218) (10 mg/kg, i.v., every other day for 7 days) or vehicle. Cardiac function was evaluated by echocardiography, and rats were euthanized to collect heart tissue for molecular analysis [5]

Absorption, Distribution and Excretion
Bioavailability after oral administration is 55%. 117-145 mL/min [Patients with B-cell chronic lymphocytic leukemia receiving a single intravenous injection of 40 mg/m²]. …Comparing the pharmacokinetics of subcutaneous and intravenous fludarabine in patients with lupus nephritis. …An open-label, randomized, crossover trial conducted concurrently with a phase I/II trial. …Government research hospital. …5 patients with lupus nephritis. …Fludarabine 30 mg/m²/day, subcutaneously or intravenously over 0.5 hours, for 3 consecutive days. All patients received oral cyclophosphamide 0.5 g/m² on the first day of each cycle. Plasma samples were collected before the first dose and at 0.5, 1, 1.5, 2, 4, 8, and 24 hours after dose. Urine samples were collected every 6 hours for 24 hours. The levels of fludarabine's major metabolite, fluoroarabinofuranofuranopurine (F-ara-A), in plasma and urine were analyzed using high-performance liquid chromatography (HPLC). Pharmacokinetics of F-ara-A were analyzed using a compartmental model, and the results showed that a linear two-compartment model best described its pharmacokinetic characteristics. The Wilcoxon signed-rank test was used to compare the pharmacokinetic differences between subcutaneous and intravenous administration. The median (interquartile range) maximum concentrations after subcutaneous and intravenous administration were 0.51 (0.38–0.56) mg/L and 0.75 (0.52–0.91) mg/L, respectively. The areas under the concentration-time curves (0–24 hours) for the two administration routes were 4.65 (4.17–4.98) mg·hr/L and 4.55 (3.5–4.94) mg·hr/L, respectively, with no significant difference between the two routes. The bioavailability of fludarabine after subcutaneous administration was approximately 105% of that after intravenous administration. There were no statistically significant differences in renal clearance and urinary excretion percentage between subcutaneous and intravenous administration. No injection site reaction was observed with subcutaneous injection. ... In patients with lupus nephritis, subcutaneous and intravenous administration of fludarabine appear to have similar pharmacokinetic characteristics. Subcutaneous administration may be a more convenient route of administration than intravenous administration.

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Biological half-life
20 hours

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Fludarabine (NSC 118218)After intravenous injection (20 mg/kg) in rats, its terminal half-life (t1/2) was 10.5 hours[2]
Fludarabine (NSC 118218)In rats, its volume of distribution (Vd) was 1.2 L/kg and its total clearance (CL) was 80 mL/min/kg[2]
Fludarabine (NSC 118218)In peripheral blood mononuclear cells, it is rapidly converted into its active metabolite fludarabine triphosphate (F-ara-ATP), reaching peak intracellular concentration 4 hours after administration[1]

Hepatotoxicity
In clinical trials, only a small number of patients with leukemia treated with fludarabine experienced elevated serum enzymes. These studies did not clarify the role of fludarabine in other anti-tumor drugs within anti-leukemia treatment regimens. There are reported cases of clinically significant liver damage caused by fludarabine, but details are limited, and most patients received other anticancer chemotherapy drugs concurrently. Fludarabine has immunosuppressive effects, reducing total white blood cell count, particularly lymphocytes and CD8 T cells. Therefore, fludarabine treatment is associated with cases of relapse of chronic hepatitis B, including some patients who were cured of hepatitis B before chemotherapy but became positive for hepatitis B surface antigen (HBsAg) after chemotherapy, accompanied by active disease, manifested as positive for hepatitis B core antibody (anti-HBc) but negative for hepatitis B surface antigen (HBsAg). Hepatitis B virus relapse usually occurs after 3 to 6 cycles of anticancer drug treatment, most commonly 2 to 4 months after the completion of chemotherapy. Due to the frequency and severity of hepatitis B virus relapse after fludarabine treatment, it is recommended that patients undergo hepatitis B surface antigen (HBsAg) and hepatitis B core antibody (anti-HBc) screening before treatment and receive prophylactic antiviral therapy with oral nucleoside antiviral drugs with potent activity against hepatitis B virus (such as lamivudine, tenofovir, or entecavir). If prophylactic treatment is not initiated, close monitoring and early initiation of antiviral therapy are necessary. Fludarabine is also associated with opportunistic infections, including hepatic herpesvirus and adenovirus infections. Probability score: E (Unproven but suspected cause of clinically significant liver damage).
Protein Binding
19-29%
Interactions
Fludarabine may increase serum uric acid levels as part of tumor lysis syndrome; dosage adjustments of antigout medications (allopurinol, colchicine, probenecid, sulfinpyrazone) may be necessary to control hyperuricemia and gout; allopurinol may be the first-line drug for preventing or reversing fludarabine-induced hyperuricemia due to the risk of uric acid nephropathy associated with the use of uricosuric antigout medications.
The leukopenic and/or thrombocytopenic effects of fludarabine may be enhanced if other medications (which/cause blood disorders/also have the same effect) are received concurrently or recently; the fludarabine dosage should be adjusted according to blood cell counts if necessary.
Additional bone marrow suppression may occur; dosage reduction may be necessary when two or more bone marrow suppressants (including radiation) are used concurrently or sequentially.
Concurrent use with fludarabine is not recommended due to the potential increased risk of fatal pulmonary toxicity. /Pentastatin/
For more complete data on interactions with fludarabine (10 in total), please visit the HSDB record page.

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Fludarabine (NSC 118218) induces myelosuppression in cells of patients with B-cell chronic lymphocytic leukemia (B-CLL) in vitro: neutrophil count decreased by 40% at a concentration of 1 μM [1]
Fludarabine (NSC 118218) has a plasma protein binding rate of 23% in human plasma [2]
In rats treated with Fludarabine (NSC 118218) (20 mg/kg, intravenous injection), serum ALT and AST levels increased by 15% (within the normal range), and no significant nephrotoxicity was observed (BUN and Cr did not change) [5]
Fludarabine (NSC 118218) (118218) (in vitro concentrations up to 10 μM) did not induce cardiomyocyte necrosis as indicated by normal LDH release [5]

[1]. Eur J Haematol . 2007 Dec;79(6):486-93.

[2]. Bioorg Med Chem . 1999 Jun;7(6):1195-200.

[3]. Int Immunopharmacol . 2006 May;6(5):715-23.

[4]. Eur J Cancer . 1996 Sep;32A(10):1766-73.

[5]. Am J Physiol Heart Circ Physiol . 2007 Jun;292(6):H2935-43.

Therapeutic Uses

Fludarabine is indicated for the treatment of patients with B-cell chronic lymphocytic leukemia (CLL) who have failed or whose disease has progressed to treatment with at least one standard regimen containing an alkylating agent. /Included in the US product label/
Fludarabine is indicated for the treatment of non-Hodgkin's lymphoma. /Not included in the US product label/
Fludarabine phosphate is a purine analogue currently used to treat low-grade lymphoid malignancies.
An updated study aimed to evaluate long-term survival in previously treated patients with chronic lymphocytic leukemia (CLL) after receiving salvage therapy with fludarabine. …From September 1992 to December 1995, 74 patients with advanced relapsed B-cell CLL were enrolled in the study. Fludarabine was administered at a dose of 25 mg/m²/day for 5 consecutive days via intravenous infusion over 30 minutes. Treatment was repeated every 28 days for a maximum of 6 cycles. …19 patients (26%) achieved complete remission (CR), and 20 patients (27%) achieved partial remission (PR), for an overall response rate of 53%. Median overall survival was 68 months, significantly negatively correlated with the number of prior treatments. Median progression-free survival was 18 months for patients achieving CR and 12 months for those achieving PR. …In this cohort of chronic lymphocytic leukemia (CLL) patients, the results of fludarabine monotherapy demonstrated significant disease-free survival. This time window can be used to consolidate the initial treatment response, employing biological approaches or high-dose treatment strategies, such as autologous bone marrow transplantation, with the ultimate goal of eradicating the disease.

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Drug Warning
Fludarabine for injection should be used under the guidance of a qualified physician with experience in antitumor therapy. Fludarabine for injection can severely suppress bone marrow function. In dose-range studies of patients with acute leukemia, high doses of fludarabine for injection were associated with severe neurological adverse reactions, including blindness, coma, and death.
This severe neurotoxicity occurred in 36% of patients receiving doses approximately four times the recommended dose (96 mg/m²/day for 5–7 days). Similar severe central nervous system toxicities, including coma, seizures, agitation, and confusion, have been reported in patients receiving treatment within the recommended dose range for chronic lymphocytic leukemia. Life-threatening and even fatal autoimmune phenomena, such as hemolytic anemia, autoimmune thrombocytopenic purpura (ITP), Evans syndrome, and acquired hemophilia, have been reported after one or more cycles of fludarabine injection. Patients receiving fludarabine injection should be evaluated for hemolysis and closely monitored. In a clinical study using fludarabine injection in combination with pentostatin (deoxycodone) for the treatment of refractory chronic lymphocytic leukemia (CLL), the incidence of fatal pulmonary toxicity was unacceptably high. Therefore, the combined use of injectable fludarabine and pentostatin is not recommended.
The bone marrow suppression effect of fludarabine may lead to an increased incidence of microbial infections, delayed wound healing, and gingival bleeding. Dental treatment should be completed before the start of treatment whenever possible, or postponed until blood cell counts return to normal. Patients should be instructed to maintain good oral hygiene during treatment, including careful use of regular toothbrushes, dental floss, and toothpicks. Fludarabine can sometimes also cause stomatitis with significant discomfort.
For more complete data on drug warnings for fludarabine (26 in total), please visit the HSDB record page.

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Pharmacodynamics
Fludarabine is a chemotherapeutic agent used to treat chronic lymphocytic leukemia. It acts on DNA polymerase α, ribonucleotide reductase, and DNA primase, leading to inhibition of DNA synthesis, thereby destroying cancer cells.

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Fludarabine (NSC 118218) is a purine nucleoside analog (2-fluoro-9-β-D-arabinofuranosyladenine) with antitumor and immunosuppressive properties [2,4].
Fludarabine (NSC 118218) exerts its antitumor effect by inhibiting DNA synthesis: its active metabolite F-ara-ATP competes with deoxyadenosine triphosphate (dATP) for incorporation into DNA, leading to chain termination [2,4].
Fludarabine (NSC 118218) induces apoptosis in malignant lymphocytes through the mitochondrial-inherent pathway (upregulating Bax, downregulating…). Bcl-2) [1]
Fludarabine (NSC 118218) alleviates myocardial hypertrophy by inhibiting the NF-κB-mediated inflammatory signaling pathway [5]
Fludarabine (NSC 118218) is clinically used to treat B-cell chronic lymphocytic leukemia and non-Hodgkin's lymphoma [1,4]

C10H12FN5O4

285.23

285.087

C, 42.11; H, 4.24; F, 6.66; N, 24.55; O, 22.44

21679-14-1

657237

White to yellow solid powder

2.2±0.1 g/cm3

747.3±70.0 °C at 760 mmHg

265-268ºC

405.8±35.7 °C

0.0±2.6 mmHg at 25°C

1.876

-0.4

139.54

4

9

2

20

367

4

FC1=NC(=C2C(=N1)N(C([H])=N2)[C@@]1([H])[C@]([H])([C@@]([H])([C@@]([H])(C([H])([H])O[H])O1)O[H])O[H])N([H])[H]

HBUBKKRHXORPQB-FJFJXFQQSA-N

InChI=1S/C10H12FN5O4/c11-10-14-7(12)4-8(15-10)16(2-13-4)9-6(19)5(18)3(1-17)20-9/h2-3,5-6,9,17-19H,1H2,(H2,12,14,15)/t3-,5-,6+,9-/m1/s1

(2R,3S,4S,5R)-2-(6-amino-2-fluoropurin-9-yl)-5-(hydroxymethyl)oxolane-3,4-diol

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: ≥ 2.5 mg/mL (8.76 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 (8.76 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 (8.76 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: 30% propylene glycol, 5% Tween 80, 65% D5W: 30 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。