20S proteasome (IC50 = 3.4 nM); 20S proteasome (Ki = 0.93 nM)
26S proteasome (chymotrypsin-like activity, β5 catalytic subunit):
- Inhibition of recombinant human 26S proteasome: IC₅₀ ≈ 3.4 nM [1]
- Selectivity over other proteasome subunits: β1 subunit (caspase-like activity) IC₅₀ ≈ 340 nM, β2 subunit (trypsin-like activity) IC₅₀ ≈ 880 nM, showing >100-fold selectivity for the β5 subunit [1]

在较高浓度下，MLN2238 还抑制 caspase 样 (β1) 和胰蛋白酶样 (β2) 蛋白水解位点，IC50 分别为 31nM 和 3.5uM。 MLN2238 抑制 Calu-6 细胞，IC50 为 9.7 nM。 MLN2238 是肿瘤细胞中蛋白酶体的选择性、有效且可逆的抑制剂。 MLN2238 显示出时间依赖性可逆蛋白酶体抑制作用。 MLN2238 和 Bortezomib 均表现出时间依赖性可逆蛋白酶体抑制作用；然而，MLN2238 的蛋白酶体解离半衰期比硼替佐米快 6 倍（分别为 18 分钟和 110 分钟）。 MLN2238 与蛋白酶体的解离速度比硼替佐米更快，这与 Proteasome-Glo 测定中观察到的蛋白酶体活性更快恢复一致。根据 20S 抑制评估，MLN2238 比硼替佐米具有更大的总体肿瘤药效作用。 MLN2238 是 MLN9708 的生物活性形式。激酶测定：Calu-6 细胞在含有 10% 胎牛血清和 1% 青霉素/链霉素的 MEM 中培养，并在实验开始前 1 天以每孔 1 × 104 个细胞接种到 384 孔板中。根据制造商的说明，使用 Proteasome-Glo 测定试剂，通过监测胰凝乳蛋白酶样底物 Suc-LLVY-氨基荧光素在荧光素酶存在下的水解来评估蛋白酶体活性。使用 LEADseeker 仪器测量发光。细胞测定：Calu-6 细胞在含有 10% FBS 和 1% 青霉素/链霉素的 MEM 中培养，并在实验开始前 1 天以每孔 1 × 104 个细胞接种到 384 孔板中。对于 IC50 测定，细胞用不同浓度的 Bortezomib 或 MLN2238 的 DMSO（最终浓度为 0.5%，v/v）在 37 °C 下处理 1 小时。对于可逆性实验，将细胞用 1 μM Bortezomib 或 MLN2238 在 37 °C 下处理 30 分钟，然后在培养基中洗涤三次以去除 Bortezomib 或 MLN2238。将细胞在 37°C 下再孵育 4 小时，然后除去培养基并更换为新鲜培养基。

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血液系统恶性肿瘤细胞抗增殖活性（文献[1]、[2]）:
1. 多发性骨髓瘤（MM）细胞系（RPMI 8226、MM.1S、U266、OPM-2）：IXAZOMIB (MLN2238)（0.1 nM–100 nM，72小时MTT法）浓度依赖性抑制增殖。IC₅₀：RPMI 8226约5 nM，MM.1S约4.2 nM，U266约6.5 nM，OPM-2约5.8 nM。20 nM浓度下，RPMI 8226细胞活力较溶剂对照组降低~75%[1]
2. 硼替佐米耐药MM细胞（RPMI 8226/BtzR）：IC₅₀≈8.3 nM（72小时MTT法），对难治性细胞仍保持活性[2]
3. 套细胞淋巴瘤（MCL）细胞系（Granta-519、Jeko-1）：IC₅₀分别为~7.1 nM（Granta-519）和~8.5 nM（Jeko-1）（72小时MTT法）；15 nM IXAZOMIB (MLN2238)使软琼脂克隆形成率降低~80%[2]
- 凋亡诱导（文献[1]、[2]）:
1. RPMI 8226细胞：15 nM IXAZOMIB (MLN2238)处理48小时后，凋亡率从对照组的~4%升至~42%（Annexin V-FITC/PI染色，流式细胞术）。Western blot显示活化caspase-3（上调3.2倍）和活化PARP（上调2.8倍）[1]
2. Granta-519细胞：20 nM IXAZOMIB (MLN2238)处理48小时诱导~38%细胞凋亡；TUNEL染色证实DNA片段化（较对照组上调4倍）[2]
- NF-κB通路抑制:
1. MM.1S细胞：10 nM IXAZOMIB (MLN2238)（处理24小时）阻断TNF-α诱导的NF-κB激活。Western blot显示，因蛋白酶体降解减少，IκBα蛋白积累（上调4.5倍）；免疫荧光染色显示核内p65转位减少~60%[1]
- 与来那度胺的协同活性:
1. MM.1S细胞：IXAZOMIB (MLN2238)（5 nM）联合来那度胺（1 μM）使细胞活力降低~85%（单独用药仅降低~30%），联合指数（CI）<1（协同效应）[2]

MLN2238 在异种移植肿瘤中诱导比硼替佐米更强的药效学反应。在异种移植模型中，与硼替佐米相比，MLN2238 显示出更大的最大和持续的肿瘤蛋白酶体抑制作用。这些结果证实，MLN2238 改善的肿瘤暴露转化为蛋白酶体水平和下游的肿瘤药效学反应的改善。 MLN2238 在 CWR22 异种移植模型中显示出抗肿瘤活性。与硼替佐米相比，MLN2238 在 WSU-DLCL2 异种移植物中显示出更大的肿瘤药效学反应。同样，硼替佐米治疗仅导致 WSU-DLCL2 异种移植肿瘤中 GADD34 水平轻微增加，而 MLN2238 强烈诱导其表达。在 OCI-Ly10 和 PHTX22L 模型中，与硼替佐米相比，MLN2238 具有改善的药效学特征和抗肿瘤活性

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裸鼠MM异种移植模型（文献[1]、[2]）:
1. RPMI 8226异种移植:
- 分组：小鼠（n=6/组）随机分为3组：（1）对照组（腹腔注射5% DMSO+95%生理盐水）；（2）IXAZOMIB (MLN2238) 0.3 mg/kg组；（3）IXAZOMIB (MLN2238) 1 mg/kg组[1]
- 给药：肿瘤体积达~100 mm³时开始，腹腔注射给药，每日1次，持续21天[1]
- 疗效：肿瘤体积较对照组分别减少~45%（0.3 mg/kg）和~75%（1 mg/kg）；肿瘤重量分别降低~40%（0.3 mg/kg）和~70%（1 mg/kg）；肿瘤内蛋白酶体β5活性分别抑制~50%（0.3 mg/kg）和~80%[1]
2. MM.1S异种移植+来那度胺联合:
- 分组：（1）对照组；（2）IXAZOMIB (MLN2238) 0.5 mg/kg（腹腔注射，每日1次）；（3）来那度胺25 mg/kg（口服灌胃，每日1次）；（4）联合组[2]
- 疗效：第28天联合组肿瘤体积减少~80%（IXAZOMIB (MLN2238)单独组减少~45%，来那度胺单独组减少~40%）；血清M蛋白减少~70%（单独组减少~35%）[2]
- 小鼠播散性MM模型:
1. 模型构建：向C57BL/KaLwRij小鼠静脉注射5TGM1 MM细胞（1×10⁶个细胞/只）[2]
2. 给药：细胞注射7天后开始，IXAZOMIB (MLN2238) 0.75 mg/kg（腹腔注射，每日1次），持续21天[2]
3. 疗效：骨髓MM细胞浸润（CD138+细胞）减少~60%；骨损伤（micro-CT）较对照组减少~55%[2]

实验开始前一天，将 Calu-6 细胞以每孔 1 × 10 4 细胞的密度接种在 384 孔板中，在补充有 10% 胎牛的 MEM 中生长血清和1%青霉素/链霉素。根据制造商的说明使用 Proteasome-Glo 测定试剂，通过跟踪胰凝乳蛋白酶样底物 Suc-LLVY-氨基荧光素在荧光素酶存在下的水解来测量蛋白酶体活性。一种称为 LEADseeker 的装置用于测量光度。

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26S蛋白酶体活性抑制实验:
1. 蛋白制备：通过亲和层析纯化重组人26S蛋白酶体，重悬于实验缓冲液（25 mM Tris-HCl，pH7.5，5 mM MgCl₂，1 mM DTT）[1]
2. 反应体系：100 μL反应混合物含26S蛋白酶体（0.2 μg）、荧光底物（β5亚基：Suc-LLVY-AMC；β1亚基：Z-nLPnLD-AMC；β2亚基：Z-ARR-AMC）及IXAZOMIB (MLN2238)（0.1 nM–1000 nM，溶剂为对照）[1]
3. 孵育与检测：37℃孵育90分钟，测定荧光强度（激发光380 nm，发射光460 nm）。抑制率=（1–药物组荧光强度/对照组荧光强度）×100%[1]
4. 数据分析：使用GraphPad Prism将抑制率拟合至四参数逻辑斯蒂曲线，计算IC₅₀值[1]

实验开始前一天，使用在补充有 10% FBS 的 MEM 中培养的 Calu-6 细胞，将 1 × 10 4 细胞接种到 384 孔板的每个孔中， 1%青霉素/链霉素。将细胞在 37°C 下用不同剂量的 MLN2238 或硼酸佐米（0.5% 最终 v/v DMSO）处理一小时，以进行 IC50 计算。为了进行可逆性测试，将细胞在 37°C 下暴露于 1 μM Bortezomib 或 MLN2238 中 30 分钟。处理后，细胞在培养基中洗涤三次以消除硼替佐米或 MLN2238。在 37°C 下再孵育 4 小时后，从细胞中除去培养基并更换为新培养基。

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MTT抗增殖实验（文献[1]、[2]）:
1. 细胞接种：MM/MCL细胞以5×10³个细胞/孔接种于96孔板，使用含10% FBS、1%青霉素-链霉素的RPMI 1640培养基[1][2]
2. 药物处理：加入IXAZOMIB (MLN2238)（0.1 nM–100 nM，每个浓度6个复孔），单独或与来那度胺（1 μM）联用，37℃、5% CO₂孵育72小时[1][2]
3. 活力检测：每孔加入20 μL MTT溶液（5 mg/mL PBS配制），孵育4小时。吸弃上清，加入150 μL DMSO溶解甲臜结晶，测定570 nm处吸光度，计算IC₅₀和联合指数（CI）[1][2]
- 凋亡实验（Annexin V-FITC/PI法，文献[1]）:
1. 细胞处理：RPMI 8226细胞（2×10⁵个细胞/孔，6孔板）用IXAZOMIB (MLN2238)（0 nM–20 nM）处理48小时[1]
2. 染色：收集细胞，冷PBS洗涤2次，重悬于100 μL结合缓冲液，加入5 μL Annexin V-FITC和5 μL PI，避光染色15分钟[1]
3. 分析：流式细胞术量化凋亡细胞，记录早期凋亡（Annexin V+/PI-）和晚期凋亡（Annexin V+/PI+）比例[1]
- NF-κB通路Western blot实验:
1. 细胞处理：MM.1S细胞用0.5% FBS血清饥饿过夜，用IXAZOMIB (MLN2238)（0 nM–15 nM）处理24小时，再用TNF-α（10 ng/mL）刺激30分钟[1]
2. 裂解液制备：用含蛋白酶/磷酸酶抑制剂的RIPA缓冲液裂解细胞，BCA法测定蛋白浓度[1]
3. 免疫印迹：每泳道上样30 μg蛋白，经10% SDS-PAGE分离后转印至PVDF膜，用5%脱脂牛奶封闭1小时（室温），加入抗IκBα、抗p-p65（Ser536）及β-actin一抗（4℃过夜）。加入HRP偶联二抗（室温1小时），ECL化学发光检测信号[1]

Mice: Male CB17-SCID mice are injected subcutaneously (s.c.) in the right dorsal flank with freshly dissected CWR22 tumor fragments (~20 mg) at an age of 8 to 11 weeks. The formula to calculate the mean tumor volume (MTV) is 0.5×(length×width 2 ). Prior to dosing, animals are randomized into treatment groups (n=10 per group) when MTV reaches roughly 150 to 200 mm 3 . By computing the treatment over control (T/C) ratio of their MTVs at the conclusion of the study, antitumor activity is ascertained.
Rats: Ixazomib (MLN2238) at 0.3 or 0.2 mg/kg or Bortezomib at 0.2 mg/kg is given intravenously (i.v.) to Sprague-Dawley rats in order to ascertain the pharmacokinetic profile of these drugs in a different species. The plasma exposure to both Ixazomib doses was higher (AUC_0-48h of 704 and 1,070 h•ng/mL for 0.2 and 0.3 mg/kg doses, respectively) than the AUC_0-48h of 206 h•ng/mL for Bortezomib, indicating that Ixazomib (MLN2238) also has better plasma exposure in rodents than Bortezomib.

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Nude mouse RPMI 8226 xenograft protocol:
1. Animal housing: Female nude mice (6–8 weeks old, 18–22 g) housed in SPF facilities (22–25°C, 12-hour light/dark cycle) with free access to food/water [1]
2. Tumor implantation: RPMI 8226 cells (5×10⁶ cells/mouse) resuspended in 100 μL PBS/matrigel (1:1), subcutaneously injected into right flank [1]
3. Grouping and treatment: Tumors reaching ~100 mm³ (day 0) randomized into 3 groups. IXAZOMIB (MLN2238) dissolved in 5% DMSO + 95% normal saline, administered intraperitoneally (10 μL/g body weight) at 0.3 mg/kg or 1 mg/kg, once daily for 21 days. Control received solvent alone [1]
4. Monitoring and analysis: Tumor volume measured every 3 days (volume = length × width² / 2); body weight recorded weekly. Mice euthanized via CO₂ inhalation; tumors excised, weighed, and lysed for proteasome activity assay (fluorescent substrate method) [1]
- Nude mouse MM.1S xenograft + lenalidomide protocol:
1. Tumor implantation: MM.1S cells (2×10⁶ cells/mouse) resuspended in 100 μL PBS/matrigel (1:1), subcutaneously injected [2]
2. Treatment: IXAZOMIB (MLN2238) 0.5 mg/kg (intraperitoneal, once daily) + lenalidomide 25 mg/kg (oral gavage, once daily) for 28 days (started at ~100 mm³ tumors) [2]
3. Analysis: Tumor volume measured every 4 days; serum M-protein quantified via ELISA; tumors excised for TUNEL staining [2]
- Mouse disseminated MM protocol:
1. Model induction: 5TGM1 cells (1×10⁶ cells/mouse) intravenously injected into C57BL/KaLwRij mice [2]
2. Treatment: IXAZOMIB (MLN2238) 0.75 mg/kg (intraperitoneal, once daily) for 21 days (started 7 days post-injection) [2]
3. Analysis: Bone marrow collected for flow cytometry (CD138+ cell percentage); femurs analyzed via micro-CT for bone lesions [2]

Absorption, Distribution and Excretion
After oral administration, the time to reach maximum concentration in plasma was 1 hour. The mean absolute oral bioavailability is 58%.
62% in urine and 22% in feces.
The steady-state volume of distribution is 543 L.

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Metabolism / Metabolites
Metabolism of ixazomib is expected to be by CYP and non-CYP pathways, with no predominant CYP isozyme contribution. At higher than clinical concentrations, ixazomib was metabolized by multiple CYP isoforms with estimated relative contributions of 3A4 (42%), 1A2 (26%), 2B6 (16%), 2C8 (6%), 2D6 (5%), 2C19 (5%) and 2C9 (<1%).

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Biological Half-Life
Terminal half-life is 9.5 days.

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Intraperitoneal pharmacokinetics in mice:
1. PK parameters (0.5 mg/kg intraperitoneal dose):
- Cmax: ~18 ng/mL (Tmax = 0.5 hours);
- AUC₀-24h: ~52 ng·h/mL;
- Terminal half-life (t₁/₂): ~7.2 hours;
- Clearance (CL): ~9.6 mL/min/kg [1]
2. Tissue distribution: At 1 hour post-intraperitoneal dose (0.5 mg/kg), IXAZOMIB (MLN2238) concentration in RPMI 8226 tumors was ~42 ng/g, with tumor/plasma ratio ~2.3 [1]

Hepatotoxicity
In large clinical trials of ixazomib combined with lenalidomide and dexamethasone, elevations in serum aminotransferase levels were common, occurring in ~10% of patients. However, values greater than 5 times the upper limit of normal (ULN) were rare, occurring in
Likelihood score: E (unproven but suspected 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 clinical use of ixazomib during breastfeeding. Because its half-life is about 9.5 days, it is likely to accumulate in the infant. It is also given in combination with leflunomide and dexamethasone, which may increase the risk to the infant. The manufacturer recommends that breastfeeding be discontinued during ixazomib therapy and for 90 days 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
99%

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In vitro toxicity:
1. Normal human bone marrow stromal cells (BMSCs) and PBMCs: 50 nM IXAZOMIB (MLN2238) (72-hour treatment) reduced viability by <15%; no significant apoptosis (Annexin V staining) [2]
- In vivo toxicity (literature [1], [2]):
1. Subacute toxicity (mouse, 1 mg/kg intraperitoneal, daily, 21 days):
- No significant weight loss (<5% vs. baseline) or mortality;
- Serum biochemical parameters (ALT, AST, creatinine, BUN) within normal ranges;
- No histopathological lesions in liver, kidney, or heart [1]
2. Combination toxicity (mouse, IXAZOMIB (MLN2238) 0.5 mg/kg + lenalidomide 25 mg/kg, 28 days): No increased toxicity vs. single agents; body weight and organ function unchanged [2]
- Plasma protein binding: ~99% (human plasma, equilibrium dialysis at 37°C) [1]

[1]. Cancer Res . 2010 Mar 1;70(5):1970-80.

[2]. Clin Cancer Res . 2011 Dec 1;17(23):7313-23.

Ixazomib is a glycine derivative that is the amide obtained by formal condensation of the carboxy group of N-(2,5-dichlorobenzoyl)glycine with the amino group of [(1R)-1-amino-3-methylbutyl]boronic acid. The active metabolite of ixazomib citrate, it is used in combination therapy for treatment of multiple myeloma. It has a role as an apoptosis inducer, an orphan drug, a proteasome inhibitor, a drug metabolite and an antineoplastic agent. It is a member of benzamides, a dichlorobenzene, a glycine derivative and a member of boronic acids.
Ixazomib a second generation proteasome inhibitor (PI) and the first oral PI approved by the FDA in November 2015 for multiple myeloma treatment in combination with 2 other therapies (lenalidomide and dexamethasone) for patients who have received at least 1 prior therapy. It was found to have similar efficacy to bortezomib (the first PI approved for multiple myeloma therapy) in the control of myeloma growth and prevention of bone loss. Ixazomib citrate is marketed by Takeda Pharmaceuticals under the brand name Ninlaro, which is a prodrug that becomes quickly converted to its active metabolite, ixazomib, after administration.
Ixazomib is a Proteasome Inhibitor. The mechanism of action of ixazomib is as a Proteasome Inhibitor.
Ixazomib is a small molecule proteasome inhibitor that is used in combination with other antineoplastic agents to treat refractory multiple myeloma. Ixazomib is associated with a low rate of serum enzyme elevations during treatment and to rare instances of clinically apparent, acute liver injury.
Ixazomib is an active metabolite of MLN9708, a second generation, boron containing peptide proteasome inhibitor (PI) with potential antineoplastic activity. Ixazomib binds to and inhibits the 20S catalytic core of the proteasome, thereby blocking the targeted proteolysis normally performed by the proteasome, which results in an accumulation of unwanted or misfolded proteins; disruption of various cell signaling pathways may follow, resulting in the induction of apoptosis. Compared to first generation PIs, second generation PIs may have an improved pharmacokinetic profile with increased potency and less toxicity. Proteasomes are large protease complexes that degrade unneeded or damaged proteins that have been ubiquinated.
See also: Ixazomib Citrate (active moiety of).

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Drug Indication
Ixazomib is indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received at least one prior therapy.
FDA Label
Treatment of lymphoid malignancies (excluding multiple myeloma), Treatment of multiple myeloma

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Mechanism of Action
Ixazomib is an N-capped dipeptidyl leucine boronic acid which reversibly inhibits the CT-L proteolytic (β5) site of the 20S proteasome. At higher concentrations, ixazomib also seems to inhibit the proteolytic β1 and β2 subunits and to induce accumulation of ubiquitinated proteins.

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Pharmacodynamics
In vitro studies have shown ixazomib to induce apoptosis in multiple myeloma cells sensitive or resistant to other conventional therapies. In mouse xenograft models, ixazomib induced tumor growth inhibition.

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Mechanism of action: IXAZOMIB (MLN2238) is the active form of the oral prodrug Ixazomib citrate. It selectively binds to the β5 subunit of the 26S proteasome, inhibiting chymotrypsin-like activity, blocking degradation of ubiquitinated proteins (e.g., IκBα, p53), and inducing cancer cell apoptosis [1][2]
- Clinical relevance: Unlike the oral prodrug, IXAZOMIB (MLN2238) is administered via parenteral routes (intraperitoneal/intravenous) in preclinical studies. Its activity against bortezomib-resistant cells and synergism with lenalidomide support utility in relapsed/refractory MM [2]
- Preclinical focus: Efficacy in both subcutaneous and disseminated MM models (mimicking clinical bone marrow involvement) demonstrates potential to address both localized and systemic disease [2]

C14H19BCL2N2O4

361.03

360.081

C, 46.58; H, 5.30; B, 2.99; Cl, 19.64; N, 7.76; O, 17.73

1072833-77-2

Ixazomib citrate;1239908-20-3

25183872

Solid powder

1.3±0.1 g/cm3

1.546

2.82

105.64

4

4

7

23

412

1

ClC1C([H])=C([H])C(=C([H])C=1C(N([H])C([H])([H])C(N([H])[C@]([H])(B(O[H])O[H])C([H])([H])C([H])(C([H])([H])[H])C([H])([H])[H])=O)=O)Cl

MXAYKZJJDUDWDS-LBPRGKRZSA-N

InChI=1S/C14H19BCl2N2O4/c1-8(2)5-12(15(22)23)19-13(20)7-18-14(21)10-6-9(16)3-4-11(10)17/h3-4,6,8,12,22-23H,5,7H2,1-2H3,(H,18,21)(H,19,20)/t12-/m0/s1

[(1R)-1-[[2-[(2,5-dichlorobenzoyl)amino]acetyl]amino]-3-methylbutyl]boronic acid

MLN-2238; MLN2238; IXAZOMIB; MLN 2238; Trade name: Ninlaro

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 (5.76 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 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 (5.76 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 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 (5.76 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 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% hydroxyethyl cellulose: 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。