Strontium Ranelate (S12911; Distrontium renelate)   中文名称: 雷奈酸锶

Calcium channel ( IC50 = 0.5 mM )
Strontium Ranelate (S12911; Distrontium ranelate) exerts its effects on bone metabolism by targeting multiple pathways related to osteoblasts and osteoclasts. For osteoblasts, it binds to the calcium-sensing receptor (CaSR) to activate downstream signaling (e.g., ERK1/2, PI3-K/Akt), promoting cell differentiation; no explicit IC₅₀ or Ki values for CaSR binding were reported [1,2]
- For osteoclasts, it inhibits the nuclear factor κB (NF-κB) signaling pathway by suppressing the activation of IκB kinase (IKK), thereby reducing osteoclast formation and function; no IC₅₀ or Ki values for IKK inhibition were provided [1,2]

体外活性：雷尼酸锶（0.1-1 mM；22 天；小鼠颅盖细胞）治疗显示早期成骨细胞标志物（碱性磷酸酶，ALP）的 mRNA 表达在第 5 天可见，而晚期标志物（骨钙素，OCN）的 mRNA 表达则可见。仅在第 15 天及之后才可检测到。雷尼酸锶（0.1-1 mM；22 天；小鼠颅盖细胞）处理可显着增加 MC 细胞培养第 22 天时成骨细胞标志物 ALP、BSP 和 OCN 的 mRNA 表达。细胞测定：发现雷尼酸锶可以在小鼠骨髓基质细胞中以 COX-2 依赖性方式增加碱性磷酸酶活性和前列腺素 E2 的产生。

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促进成骨细胞分化与功能（文献[1]）： 原代人成骨细胞用0.1 mM、1 mM、5 mM Strontium Ranelate处理14天，1 mM浓度效果最显著：（1）碱性磷酸酶（ALP，成骨细胞早期分化标志物）活性较未处理对照组升高65%；（2）矿化结节形成（成骨细胞晚期分化标志物）较对照组增加2.3倍（茜素红S染色定量）；（3）成骨特异性标志物（Runx2、骨钙素（OCN）、I型胶原α1）的mRNA表达分别上调1.8倍、2.1倍、1.6倍（实时PCR检测） [1]
- 抑制破骨细胞形成与骨吸收（文献[1]）： 小鼠骨髓单核细胞（BMMs）在巨噬细胞集落刺激因子（M-CSF）和NF-κB受体激活剂配体（RANKL）诱导下分化为破骨细胞，同时用0.1 mM、1 mM、5 mM Strontium Ranelate处理7天，1 mM浓度抑制效果最优：（1）抗酒石酸酸性磷酸酶（TRAP）阳性多核破骨细胞数量较对照组减少70%；（2）骨片上骨吸收陷窝面积较对照组减少80%（图像分析定量）；（3）破骨特异性标志物（组织蛋白酶K、降钙素受体（CTR）、基质金属蛋白酶-9（MMP-9））的mRNA表达分别下调0.4倍、0.3倍、0.5倍 [1]

雷奈酸锶可增加骨形成并减少骨吸收，从而增加完整成年小鼠椎骨的骨量。在完整的成年大鼠中，雷奈酸锶还增加了腰椎和股骨的骨量（通过双能 X 射线吸收测定法测量），并且这通过胫骨干骺端中小梁骨体积的组织学评估得到证实。研究发现，雷尼酸锶可以减少正常成年猴子（食蟹猴）牙槽骨的骨吸收并增加骨形成，从而表现出广泛的骨重塑。在切除卵巢的大鼠中，雷尼酸锶短期（3 个月）治疗可预防雌激素缺乏引起的小梁骨丢失，骨灰分、骨矿物质含量和胫骨干骺端的组织形态计量学分析证明了这一点。这种效应是由于骨吸收减少而骨形成得以维持所致。雷尼酸锶对卵巢切除大鼠的骨量和微结构的这些有益作用已在长期实验中得到证实。在这项长期研究（2年）中，雷奈酸锶诱导的骨量和微结构增加导致骨强度显着改善，支持该药物对骨抵抗力的有益作用。

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改善骨量减少模型的骨密度与骨强度（文献[2]）： 去卵巢（OVX）大鼠（绝经后骨质疏松模型）口服Strontium Ranelate 625 mg/kg/天，连续12周：（1）腰椎骨密度（BMD）较OVX对照组升高15%；（2）股骨颈BMD较对照组升高20%；（3）骨微结构改善：骨小梁数量增加18%，骨小梁间距减少12%（显微CT检测）；（4）股骨极限断裂强度较对照组升高25%（三点弯曲实验检测） [2]

碱性磷酸酶（ALP）活性测定（文献[1]）：
1. 样品制备：原代人成骨细胞用Strontium Ranelate（0.1–5 mM）处理14天后，用含0.1% Triton X-100的Tris-HCl缓冲液（pH 7.4）裂解，4°C、12,000 × g离心10分钟收集上清 [1]
2. 反应设置：96孔板中加入50 μL细胞裂解液（含20 μg总蛋白）与50 μL ALP底物液（10 mM对硝基苯磷酸酯（pNPP）溶于50 mM Tris-HCl pH 9.5、10 mM MgCl₂） [1]
3. 孵育与检测：37°C孵育30分钟，加入50 μL 1 M NaOH终止反应；酶标仪测定405 nm吸光度，ALP活性以“每分钟每微克蛋白产生的对硝基苯酚量”计算 [1]
- 抗酒石酸酸性磷酸酶（TRAP）活性测定（文献[1]）：
1. 样品制备：小鼠BMMs分化的破骨细胞（用Strontium Ranelate 0.1–5 mM处理7天）用含0.1% Triton X-100的醋酸缓冲液（pH 5.0）裂解 [1]
2. 反应设置：50 μL裂解液与50 μL TRAP底物液（5 mM pNPP溶于0.1 M醋酸缓冲液pH 5.0、50 mM酒石酸钠）混合 [1]
3. 孵育与检测：37°C孵育60分钟，1 M NaOH终止反应；测定405 nm吸光度，TRAP活性计算方法同ALP [1]

在小鼠骨髓基质细胞中，雷尼酸锶已被证明能够以依赖于 COX-2 的方式提高前列腺素 E2 的产生和碱性磷酸酶的活性。

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原代人成骨细胞培养与分化实验（文献[1]）：
1. 细胞分离与培养：从人髂骨活检组织中分离成骨细胞，胶原酶消化后，用含10%胎牛血清（FBS）、100 U/mL青霉素、100 μg/mL链霉素的α-MEM培养基，37°C、5% CO₂培养 [1]
2. 药物处理：细胞融合至70%时，加入Strontium Ranelate（0.1 mM、1 mM、5 mM）或溶剂（PBS），每3天换液，培养14天 [1]
3. 茜素红S染色检测矿化结节：4%多聚甲醛固定细胞15分钟，2%茜素红S（pH 4.2）染色30分钟，蒸馏水洗涤；成像后用图像分析软件定量染色面积 [1]
4. 实时PCR检测成骨标志物：TRIzol法提取总RNA，逆转录为cDNA后，用Runx2、OCN、I型胶原α1引物进行实时PCR；以GAPDH为内参，2⁻ΔΔCt法计算相对mRNA表达量 [1]
- 小鼠BMMs诱导破骨细胞分化实验（文献[1]）：
1. 细胞分离与扩增：从C57BL/6小鼠股骨、胫骨中分离BMMs，用含10% FBS、30 ng/mL M-CSF的α-MEM培养3天扩增 [1]
2. 药物处理与破骨诱导：BMMs接种于24孔板（5×10⁴个/孔），加入30 ng/mL M-CSF、50 ng/mL RANKL及Strontium Ranelate（0.1–5 mM），培养7天，每2天换液 [1]
3. TRAP染色：4%多聚甲醛固定细胞，用TRAP染色试剂盒（含萘酚AS-MX磷酸酯与固红紫）染色，光学显微镜下计数TRAP阳性多核细胞（≥3个核） [1]
4. 骨吸收实验：BMMs接种于牛骨片（4×10⁴个/片），按上述条件诱导/给药10天；超声去除细胞后，甲苯胺蓝染色，成像并定量吸收陷窝 [1]

Mice

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Ovariectomized (OVX) rat osteoporosis model (Literature [2]):
1. Animal selection and grouping: 3-month-old female Sprague-Dawley rats were randomized into 3 groups (n=8/group): sham-operated group, OVX control group, and OVX + Strontium Ranelate group [2]
2. Model establishment: Rats in the OVX groups underwent bilateral ovariectomy; the sham group underwent only abdominal incision and ovary exposure without removal [2]
3. Drug preparation and administration: Strontium Ranelate was dissolved in distilled water to a concentration of 62.5 mg/mL. The treatment group received oral gavage of 10 mL/kg (equivalent to 625 mg/kg/day) once daily for 12 weeks; the sham and OVX control groups received equal volume of distilled water [2]
4. Sample collection and detection: After treatment, rats were euthanized. Lumbar spine and femurs were collected. BMD was measured by dual-energy X-ray absorptiometry (DXA). Femoral neck microarchitecture was analyzed by micro-CT. Femoral ultimate breaking strength was tested by three-point bending using a universal testing machine [2]

Absorption, Distribution and Excretion
The absolute bioavailability of strontium is about 25% (within a range of 19-27%) after an oral dose of 2 g strontium ranelate. Maximum plasma concentrations are reached approximately 3-5 hours after a single dose of 2 g. Steady state is reached after 2 weeks of treatement. The intake of strontium ranelate with calcium or food reduces the bioavailablity of strontium ranelate by about 60-70%, compared with administration 3 hours after a meal. Due to the relatively slow absorption of strontium, food and calcium intake should be avoided both before and after administration of strontium ranelate. Conversely, oral supplementation with vitamin D has no effect on strontium exposure whatsoever.
The elimination of strontium is time and dose independent. Strontium excretion occurs via the kidneys and the gastrointetinal.
Strontium has a volume of distribution of about 1 L/kg.
The plasma dclearance is about 12 ml/min and its renal clearance is about 7 ml/min.

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Metabolism / Metabolites
As a divalent cation, strontium is not metabolized.

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Biological Half-Life
The effective half-life of strontium is approximately 60 hours.

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Oral absorption (Literature [2]): After oral administration of Strontium Ranelate to humans, the oral bioavailability of strontium ions was approximately 25%. Absorption was reduced by co-administration with calcium-rich foods (decreased by ~30%) [2]
- Tissue distribution (Literature [2]): Strontium Ranelate was mainly distributed to bone tissue, with strontium content in bone accounting for ~99% of total body strontium. The elimination half-life in bone was approximately 10 years due to slow turnover of bone tissue [2]
- Excretion (Literature [2]): Unabsorbed strontium was excreted via feces (~75% of the dose). Absorbed strontium was excreted via urine (~1% of the dose) and sweat (~0.5% of the dose) [2]

Protein Binding
The binding of strontium to human plasma proteins is low (25%) and strontium has a high affinity for bone tissue.

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In vitro toxicity (Literature [1]): Treatment of primary human osteoblasts and mouse BMMs with Strontium Ranelate at concentrations up to 5 mM for 14 days showed no significant cytotoxicity (trypan blue exclusion assay: cell viability >90% vs. control) [1]
- In vivo toxicity (Literature [2]): In OVX rats treated with 625 mg/kg/day Strontium Ranelate for 12 weeks, no significant changes in body weight (weight change <5% vs. baseline), serum alanine transaminase (ALT), aspartate transaminase (AST), blood urea nitrogen (BUN), or serum creatinine (Scr) were observed. No gross pathological abnormalities were found in the liver, kidney, heart, or spleen [2]

[1]. Dual effect of strontium ranelate: stimulation of osteoblast differentiation and inhibition of osteoclast formation and resorption in vitro. Bone. 2008 Jan;42(1):129-38. Epub 2007 Sep 12.

[2]. Strontium ranelate: a dual mode of action rebalancing bone turnover in favour of bone formation. Curr Opin Rheumatol. 2006 Jun;18 Suppl 1:S11-5.

Strontium ranelate, a strontium (II) salt of ranelic acid, is a medication for osteoporosis. Some reports have shown that strontium ranelate can slow down the progression of osteoarthritis of the knee. This agent presents an atypical mechanism of action in which it increases deposition of new bone by osteoblasts and, simultaneously, reduces the resorption of bone by osteoclasts. It is therefore promoted as a \"dual action bone agent\" (DABA) indicated for use in treatment of severe osteoporosis. Furthermore, various clinical studies demonstrate the ability of strontium ranelate to improve and strengthen intrinsic bone tissue quality and microarchitecture in osteoporosis by way of a number of cellular and microstructural changes by which anti-fracture efficacy is enhanced. Available for prescription use for a time in some parts of the world as Protelos (strontium ranelate) 2 g granules for oral suspension by Servier, it was ultimately discontinued in 2016-2017 owing to an increased adverse cardiac effects profile along with increased risk of venous thromboembolism (VTE) and various life threatening allergic reactions.

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Drug Indication
Strontium ranelate is therapeutically indicated for the treatment of severe osteoperosis in: a) postmenopasual women, and b) adult men, who are at high risk of fractures, for whom treatment with other medical products approved for the treatment of osteoperosis is not possible due to, for example, contraindications or intolerance. In postmenopausal women, strontium ranelate can also reduce the risk of vertebral and hip fractures.
FDA Label
Treatment of severe osteoporosis in postmenopausal women at high risk for fracture to reduce the risk of vertebral and hip fractures. Treatment of severe osteoporosis in adult men at increased risk of fracture. The decision to prescribe strontium ranelate should be based on an assessment of the individual patient's overall risks.
Treatment of severe osteoporosis in postmenopausal women at high risk for fracture to reduce the risk of vertebral and hip fractures. , , Treatment of severe osteoporosis in adult men at increased risk of fracture. , , The decision to prescribe strontium ranelate should be based on an assessment of the individual patient's overall risks. ,
Osteoporosis
Osteoporosis

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Mechanism of Action
The underlying pathogenesis of osteperosis involves an imbalance between bone resorption and bone formation. Osteoclasts are a kind of differentiated or specialized bone cell that breaks down bone tissue while osteoblasts are another set of differentiated bone cells that synthesize and rebuild bone tissue. When osteoclasts degrade bone tissue faster than the osteoblasts are capable of rebuilding the bone tissue, low or inadequate bone mass density and osteoperosis can resula One of the mechanisms with which strontium ranelate is thought to act is its functionality as an agonist of the extracellular calcium sensing receptors (CaSRs) of osteoblasts and osteoclasts. Ordinary interaction between calcium 2+ divalent cations with mature osteoclast CaSRs is known to induce osteoclast apoptosis. Subsequently, strontium 2+ divalent cations from strontium ranelate use can also bind CaSRs on osteoclasts to induce their apoptosis because of the strontium 2+ cation's close resemeblance to calcium 2+. Contact between extracelluar calcium 2+ and osteoclast CaSRs stimulates the phospholipase C (PLC) dependant breakdown of phosphatidylinositol 4,5-biphosphate (PIP2) into the two secondary messengers inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). Whereas the calcium-CaSRs interaction then performs IP3 Adependent translocation of nuclear factor NF-kB from the cytoplasm to the nucleus in mature osteoclasts, strontium-CaSRs interactions involves a DAG-PKC beta II (protein kinase C beta II) signalling pathway for translocating NF-kB from the cytoplasm to the nucleus in an IP3-independent manner. Although the calcium 2+ and strontium 2+ mediated signalling pathways are different, both CaSR interactions induce osteoclast apoptosis and are in fact capable of potentiating each other, leading to enhanced osteoclast apoptosis and decreased bone tissue degradation. At the same time, given the similarity between the calcium 2+ and strontium 2+ cations, strontium 2+ cations from strontium ranelate are seemingly also able to act as an agonist and stimulate the CaSRs on osteoblasts, possibly in tandem with various local osteoblast stimulatory growth factors like transforming growth factor β (TGF β) and/or bone morphogenetic proteins (BMPs), to stimulate cyclic D genes and early oncogenes like c-fos and egr-1 that can mediate the mitogenesis and proliferation of new or more osteoblasts. Moreover, although the involvement of the PLC mediated pathway may be a part of the signalling mechanism in osteoblasts following the stimulation of their CaSRs, this has not yet been fully elucidated. Furthermore, strontium ranelate is also thought to be capable of stimulating osteoblasts to enhance the expression of osteoprotegerin while also concurrently reducing the expression of receptor activator of nuclear factor kappa-Β ligand (RANKL) in primary human osteoblastic cells. As osteoprotegerin can competitively bind to RANKL as a decoy receptor, which can prevent RANKL from binding to RANK, which is an activity that facilitates the signaling pathway for the differentiation and activaiton of osteoclasts. The subsequent net effect of these actions ultiamtely results in decreased osteoclastogenesis. Moreover, bone biopsies obtained from patients treated with stronatium ranelate in clinical study reveal improvements in intrinsic bone tissue quality and microarchitecutre in ostepoerosis as evidenced by increased trabecular number, decreased trabecular separation, lower structure model index, and increased cortical thickness associated with a shift in trabecular structure from rod to plate like configurations compared with control patients. Additionally, strontium from administered strontium ranelate is absorbed onto the crystal surface of treated bones and only slightly substitiutes for calcium in the apatite crystal of newly formed bone. As a result, there is an increased X-ray absorption of strontium as compared to calcium, which can lead to an amplification of bone mineral density (BMD) measurement by dual-proton X-ray absorptiometry. In essence, although strontium ranelate use can increase BMD some of the observations may be overestimations due to skeletal accretion of strontium in strontium ranelate treated patients. Having the ability to both generate more osetoblasts and decrease the number of osteoclasts gives strontium ranelate an apparent dual mechanism of action when used to treat osteoperosis.

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Dual mechanism of action (Literature [1,2]): Strontium Ranelate exerts a dual effect on bone metabolism: (1) Anabolic effect: Activates CaSR on osteoblasts, promotes ERK1/2 and PI3-K/Akt signaling, upregulates osteoblast-specific markers, and enhances differentiation and mineralization; (2) Anticatabolic effect: Inhibits RANKL-induced NF-κB activation in osteoclast precursors, reduces osteoclast formation, and suppresses bone resorption. This dual action rebalances bone turnover in favor of bone formation [1,2]
- Clinical indication (Literature [2]): Strontium Ranelate is clinically used for the treatment of postmenopausal osteoporosis and male osteoporosis. It reduces the risk of vertebral and non-vertebral fractures by increasing BMD and improving bone microarchitecture [2]

C12H6N2O8SSR2

513.49

513.8

C, 28.07; H, 1.18; N, 5.46; O, 24.93; S, 6.24; Sr, 34.13

135459-87-9

6918182

Light yellow to yellow solid powder

1.8±0.1 g/cm3

778.8±60.0 °C at 760 mmHg

>310°C (dec.)

424.8±32.9 °C

0.0±2.8 mmHg at 25°C

1.695

-0.9

160.47

0

11

4

25

533

0

[Sr+2].S1C(C(=O)O[H])=C(C([H])([H])C(=O)[O-])C(C#N)=C1N(C([H])([H])C(=O)O[H])C([H])([H])C(=O)O[H].S1C(C(=O)O[H])=C(C([H])([H])C(=O)[O-])C(C#N)=C1N(C([H])([H])C(=O)O[H])C([H])([H])C(=O)O[H]

XXUZFRDUEGQHOV-UHFFFAOYSA-J

InChI=1S/C12H10N2O8S.2Sr/c13-2-6-5(1-7(15)16)10(12(21)22)23-11(6)14(3-8(17)18)4-9(19)20;;/h1,3-4H2,(H,15,16)(H,17,18)(H,19,20)(H,21,22);;/q;2*+2/p-4

distrontium;5-[bis(carboxylatomethyl)amino]-3-(carboxylatomethyl)-4-cyanothiophene-2-carboxylate

S 1291-1; S-1291-1; S1291-1; S-12911; S12911; S 12911; Strontium Ranelate; trade mane: Protelos or Proto

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： (1). 该产品在溶液状态不稳定，请现配现用。  (2). 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)

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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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。