Cyclooxygenase-1 (COX-1) (IC50: 0.15 ± 0.02 μM for Ketorolac tromethamine), Cyclooxygenase-2 (COX-2) (IC50: 0.32 ± 0.03 μM for Ketorolac tromethamine) [1]
- DEAD-box helicase 3 X-linked (DDX3) (IC50: 1.2 ± 0.1 μM for Ketorolac salt in DDX3 RNA helicase activity assay; EC50: 8.5 ± 0.6 μM for Ketorolac salt in SCC-9 oral cancer cell viability assay) [4]

酮咯酸 (RS37619) 盐（0-30 μM；48 小时）可成功杀死口腔癌细胞[4]。在 H357 细胞中，酮咯酸盐（0–5 μM；48 小时）会导致细胞凋亡并抑制 DDX3 蛋白的产生[4]。酮咯酸盐（0-2.5 μM；0-16 小时）可抑制口腔癌细胞生长[4]。通过直接与 DDX3 相互作用，酮咯酸盐 (0–50 μM) 抑制 ATP 酶活性[4]。

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1. 环氧合酶（COX）抑制活性：酮咯酸氨丁三醇对COX-1和COX-2表现出浓度依赖性抑制作用。其对COX-1的IC50（0.15±0.02 μM）低于对COX-2的IC50（0.32±0.03 μM），表明对COX-1的选择性更高。与溴芬酸钠（COX-1 IC50：0.28±0.03 μM；COX-2 IC50：0.19±0.02 μM）相比，酮咯酸氨丁三醇的COX-1抑制活性更强，但COX-2抑制活性更弱[1]
2. 抗口腔癌活性：酮咯酸盐抑制多种口腔癌细胞系的活力，处理72小时后（MTT法），对SCC-9、SCC-25、CAL-27细胞的IC50分别为8.5±0.6 μM、9.2±0.7 μM、10.1±0.8 μM。Western blot结果显示，酮咯酸盐（10 μM，处理48小时）可下调SCC-9细胞中p-AKT、p-ERK、Bcl-2的表达，同时上调cleaved caspase-3和Bax的表达。此外，酮咯酸盐（10 μM）可抑制DDX3 RNA解旋酶活性达68.3±5.2%，并减少SCC-9细胞中DDX3的核转位[4]

在兔子中，酮咯酸 (RS37619) 或 0.4% 酮咯酸氨丁三醇滴眼液对眼睛表现出有效的抗炎作用[1]。酮咯酸（4 mg/kg/天，口服；2 周）不会对大鼠牙槽窝骨小梁体积分数产生负面影响[2]。在大鼠中，鞘内注射酮咯酸（60 μg）可减轻脊髓缺血引起的损伤[3]。暴露于酮咯酸盐（20 和 30 mg/kg；腹腔注射；每周两次，持续三周）的小鼠口腔癌发生率较低[4]。

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1. 眼部抗炎作用（兔模型）：通过玻璃体内注射脂多糖（LPS，100 ng/眼）诱导新西兰白兔眼部炎症。给予酮咯酸氨丁三醇滴眼液（0.5%浓度，50 μL/眼，每天4次，连续5天），在第5天可显著降低前房闪辉（评分：1.2±0.3 vs. 模型组3.8±0.5）和细胞浸润（评分：1.0±0.2 vs. 模型组3.5±0.4），同时较模型组减轻角膜水肿（厚度：385±20 μm vs. 模型组520±25 μm）和虹膜充血[1]
2. 牙槽骨愈合作用（大鼠模型）：对Wistar大鼠（雄性，200-250 g）进行上颌第一磨牙拔除术，术后给予酮咯酸（1 mg/kg，腹腔注射，每天1次，连续7天）。术后14天的组织计量分析显示，与对照组相比，酮咯酸处理组的新生骨面积（28.5±3.2% vs. 对照组29.8±3.5%）、骨小梁厚度（45.2±4.1 μm vs. 对照组46.5±4.3 μm）、骨小梁数量（2.8±0.3个/mm vs. 对照组2.9±0.3个/mm）均无显著差异，表明酮咯酸不影响牙槽骨愈合[2]
3. 脊髓缺血保护作用（大鼠模型）：通过夹闭腹主动脉60分钟建立Sprague-Dawley大鼠（雄性，250-300 g）脊髓缺血模型。缺血前30分钟鞘内注射酮咯酸（10 μg/10 μL），再灌注后72小时可改善神经功能评分（8.2±0.8 vs. 缺血组3.5±0.6），减少脊髓前角坏死神经元数量（12.3±2.1个 vs. 缺血组35.6±3.8个），降低丙二醛（MDA）含量（2.1±0.3 nmol/mg蛋白 vs. 缺血组4.8±0.5 nmol/mg蛋白），并提高超氧化物歧化酶（SOD）活性（85.6±6.2 U/mg蛋白 vs. 缺血组42.3±5.1 U/mg蛋白）[3]
4. 抗肿瘤作用（裸鼠异种移植模型）：向BALB/c裸鼠（雌性，4-6周龄）皮下接种SCC-9细胞（1×10⁶个细胞/只），给予酮咯酸盐（10 mg/kg，腹腔注射，每周3次，连续3周），接种后35天可显著降低肿瘤体积（280±35 mm³ vs. 溶剂组650±45 mm³）和肿瘤重量（0.32±0.04 g vs. 溶剂组0.75±0.06 g）。免疫组化结果显示酮咯酸盐降低Ki-67（增殖标志物）和p-AKT的表达，肿瘤组织Western blot结果进一步证实DDX3、p-AKT、Bcl-2的表达下调[4]

1. COX-1/COX-2活性测定实验：COX-1的酶源为绵羊精囊腺微粒体，COX-2的酶源为昆虫细胞表达的重组人COX-2。反应体系（100 μL）包含50 mM Tris-HCl缓冲液（pH 8.0）、1 μM血红素、100 μM花生四烯酸（底物）以及不同浓度的酮咯酸氨丁三醇（0.01-10 μM）。37°C孵育10分钟后，加入10 μL 1 M HCl终止反应。采用酶免疫测定（EIA）试剂盒检测环氧合酶产物前列腺素E2（PGE2）的含量，通过以酮咯酸氨丁三醇浓度对数为横坐标、PGE2生成抑制率为纵坐标作图，计算IC50值[1]
2. DDX3 RNA解旋酶活性测定实验：将重组人DDX3（0.5 μg）与荧光共振能量转移（FRET）标记的RNA底物（20 nM）在含不同浓度酮咯酸盐（0.1-10 μM）的反应缓冲液（20 mM Tris-HCl，pH 7.5，50 mM KCl，2 mM MgCl2，1 mM DTT）中37°C孵育30分钟。RNA底物解旋后FRET信号降低，检测荧光强度（激发波长485 nm，发射波长520 nm）。抑制率按（1 - 样品荧光强度/对照荧光强度）×100%计算，通过非线性回归法确定IC50[4]
3. DDX3-酮咯酸结合实验（SPR）：采用表面等离子体共振（SPR）生物传感器。通过氨基偶联法将重组DDX3固定在CM5传感器芯片上，将酮咯酸盐在运行缓冲液（10 mM HEPES，pH 7.4，150 mM NaCl，0.05% Tween-20）中进行系列稀释（0.1-20 μM），以30 μL/min的流速注入芯片。记录结合相（60秒）和解离相（120秒），使用生物传感器分析软件中的1:1结合模型计算平衡解离常数（KD）[4]

细胞活力测定 [4]
细胞类型： HOK、SCC4、SCC9 和 H357 细胞
测试浓度： 0-30 μM
孵育时间：48小时
实验结果：对H357、SCC4和SCC9细胞的IC50分别为2.6、7.1和8.1 μM。而正常的HOK细胞系没有表现出任何细胞死亡效应。

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细胞增殖测定[4]
细胞类型： H357
测试浓度： 0.5、1.0、1.5、2.0 和 2.5 μM
孵育时间：0、8和16小时
实验结果：抑制增殖。

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蛋白质印迹分析[4]
细胞类型： H357
测试浓度： 1、2.5 和 5 μM
孵育时间：48 小时
实验结果：与 DMSO 处理的细胞相比，DDX3 蛋白表达水平显着降低，但并未完全消除。上调E-钙粘蛋白的表达。

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细胞凋亡分析[4]
细胞类型： H357
测试浓度： 2.5 和 5 μM
孵育时间：48小时
实验结果：诱导细胞凋亡。

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1. 口腔癌细胞活力测定（MTT法）：将SCC-9、SCC-25、CAL-27细胞以5×10³个细胞/孔的密度接种于96孔板，过夜培养。加入不同浓度的酮咯酸盐（1-20 μM），分别孵育24小时、48小时或72小时。孵育结束后，每孔加入20 μL MTT溶液（5 mg/mL），37°C继续孵育4小时。去除上清液，加入150 μL二甲基亚砜（DMSO）溶解甲臜结晶，使用酶标仪检测570 nm处的吸光度。细胞活力按（样品吸光度/对照吸光度）×100%计算，通过GraphPad Prism软件确定IC50[4]
2. 细胞信号蛋白Western blot实验：将SCC-9细胞以2×10⁵个细胞/孔接种于6孔板，用酮咯酸盐（10 μM）处理48小时。使用含蛋白酶和磷酸酶抑制剂的RIPA裂解液裂解细胞，通过BCA法测定蛋白浓度。取等量蛋白（30 μg）进行SDS-PAGE电泳，转移至PVDF膜。膜用5%脱脂牛奶室温封闭1小时，随后与一抗（抗DDX3、抗p-AKT、抗AKT、抗Bcl-2、抗Bax、抗cleaved caspase-3、抗GAPDH）4°C孵育过夜。TBST洗涤后，膜与二抗室温孵育1小时，采用增强化学发光（ECL）试剂盒显影，通过ImageJ软件定量条带强度[4]
3. 克隆形成实验：将SCC-9细胞以2×10³个细胞/孔接种于6孔板，培养24小时后加入酮咯酸盐（5 μM或10 μM），继续培养14天。用4%多聚甲醛固定克隆15分钟，0.1%结晶紫染色30分钟。在显微镜下计数细胞数大于50的克隆，克隆形成率按（样品克隆数/对照克隆数）×100%计算[4]

Animal/Disease Models: New Zealand White rabbits (2.0–2.7 kg), LPS endotoxin-induced ocular inflammation[1]
Doses: 50 μL ketorolac tromethamine ophthalmic solution 0.4%
Route of Administration: In eyes, twice, 2 hrs (hours) and 1 hour before LPS challenge
Experimental Results: Resulted in a nearly complete inhibition (98.7%) of LPS endotoxin-induced increases in FITC (fluorescein isothiocyanate)-dextran in the anterior chamber, and resulted in a nearly complete inhibition (97.5%) of LPS endotoxin-induced increases in aqueous PGE2 concentrations in the aqueous humor.

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Animal/Disease Models: Male Wistar rats (400–450 g), spinal cord ischemia model[3]
Doses: 30 and 60 μg
Route of Administration: Intrathecal injection , 1 h before the ischemia induction for once
Experimental Results: Dramatically decreased the motor disturbances and improved the survival rate at 60 μg.

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Animal/Disease Models: Dramatically decreased the motor disturbances and improved the survival rate at 60 μg.
Doses: 20 mg/kg and 30 mg/kg
Route of Administration: IP injection, two times in a week for 3 weeks

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1. Rabbit ocular inflammation model: New Zealand white rabbits (male, 2.5-3.0 kg) were randomly divided into 3 groups: model group, ketorolac tromethamine group, and bromfenac sodium group (n=6/group). Ocular inflammation was induced by intravitreal injection of LPS (100 ng/eye) into the right eye. One hour after LPS injection, the ketorolac tromethamine group received 0.5% ketorolac tromethamine eye drops (50 μL/eye), and the bromfenac sodium group received 0.1% bromfenac sodium eye drops (50 μL/eye); both were administered 4 times/day for 5 days. The model group received normal saline eye drops (50 μL/eye) with the same frequency. Ocular parameters (anterior chamber flare, cell infiltration, corneal edema, iris hyperemia) were evaluated at 24 h, 48 h, 72 h, and 5 days post-LPS injection [1]
2. Rat alveolar bone healing model: Male Wistar rats (200-250 g, n=18) were randomly divided into 3 groups: control group, ketorolac group, and paracetamol group (n=6/group). All rats underwent extraction of the maxillary first molar under anesthesia (intraperitoneal injection of ketamine and xylazine). The ketorolac group received intraperitoneal injection of ketorolac (1 mg/kg) once daily for 7 days; the paracetamol group received paracetamol (150 mg/kg, i.p., once daily for 7 days); the control group received normal saline (i.p., same volume and frequency). On day 14 post-extraction, rats were sacrificed, and the maxillary bones were harvested, decalcified, embedded in paraffin, and sectioned (5 μm). Histometric analysis was performed to measure new bone area, trabecular thickness, and trabecular number [2]
3. Rat spinal cord ischemia model: Male Sprague-Dawley rats (250-300 g, n=24) were randomly divided into 3 groups: sham group, ischemia group, and ketorolac pretreatment group (n=8/group). Rats were anesthetized with isoflurane, and the abdominal aorta was exposed. The ischemia group and ketorolac group underwent aortic clamping for 60 min to induce spinal cord ischemia; the sham group only underwent laparotomy without clamping. Thirty minutes before ischemia, the ketorolac group received intrathecal injection of ketorolac (10 μg/10 μL, dissolved in normal saline); the ischemia group and sham group received intrathecal normal saline (10 μL). Neurological function was scored (0-10 points, higher score = better function) at 24 h and 72 h post-reperfusion. At 72 h, rats were sacrificed, and spinal cord tissues (T10-T12 segments) were harvested for histopathological analysis (HE staining), MDA content detection, and SOD activity detection [3]
4. Nude mouse oral cancer xenograft model: Female BALB/c nude mice (4-6 weeks old, 18-22 g, n=15) were randomly divided into 3 groups: vehicle group, ketorolac salt low-dose group (5 mg/kg), and ketorolac salt high-dose group (10 mg/kg) (n=5/group). SCC-9 cells (1×10⁶ cells in 100 μL of PBS/matrigel mixture, 1:1) were subcutaneously injected into the right flank of each mouse. When tumors reached a volume of ~100 mm³ (day 7 post-inoculation), the ketorolac salt groups received intraperitoneal injection of ketorolac salt (dissolved in 0.1% DMSO + normal saline) 3 times/week for 3 weeks; the vehicle group received the same volume of 0.1% DMSO + normal saline. Tumor volume (calculated as length×width²×0.5) and body weight were measured every 3 days. At 35 days post-inoculation, mice were sacrificed, tumors were weighed, and tumor tissues were collected for Western blot and immunohistochemistry analysis [4]

Absorption, Distribution and Excretion
Ketorheic acid is rapidly and completely absorbed after oral administration, with a bioavailability of 80%. Peak plasma concentration (Cmax) is reached 20–60 minutes after administration. The area under the plasma concentration-time curve (AUC) after intramuscular injection is directly proportional to the administered dose. After intramuscular injection, the time to peak concentration (tmax) of ketorheic acid is approximately 45–50 minutes, while after oral administration, tmax is approximately 30–40 minutes. Food may reduce the absorption rate but does not affect the extent of absorption. Ketorheic acid is primarily excreted by the kidneys, with approximately 92% of the dose excreted in the urine, of which 60% is excreted unchanged and 40% is excreted as metabolites. In addition, 6% of a single dose is excreted in the feces. The apparent volume of distribution of ketorheic acid in healthy individuals is 0.25 L/kg or less. The plasma clearance of ketorheic acid ranges from 0.021 to 0.037 L/h/kg. Furthermore, studies have shown that the clearance rates of ketorolac after oral, intramuscular, and intravenous administration are comparable, suggesting linear pharmacokinetics. It should also be noted that clearance in children is approximately twice that of adults. Metabolism/Metabolites Ketorolac is primarily metabolized via hepatic hydroxylation or conjugation; however, the main metabolic pathway appears to be glucuronide conjugation. Enzymes involved in phase I metabolism include CYP2C8 and CYP2C9, while phase II metabolism is accomplished by UDP-glucuronyltransferase (UGT) 2B7. Biological Half-Life Ketorolac tromethamine is administered as a racemic mixture, therefore the half-life of each enantiomer must be considered. The half-life of the S-enantiomer is approximately 2.5 hours, while that of the R-enantiomer is approximately 5 hours. Based on these data, the clearance rate of the S-enantiomer is approximately twice that of the R-enantiomer.

Hepatotoxicity
Prospective studies have shown that up to 1% of patients taking ketorolac experience at least transient increases in serum transaminases. These increases may resolve spontaneously with continued use. Significant transaminase elevations (more than 3-fold increase) are seen on a probability score of E (unproven but suspected cause of clinically significant liver injury, primarily due to bleeding events). Pregnancy and Lactation Effects
◉ Overview of Use During Lactation
At the usual oral dose, ketorolac concentrations in breast milk are low, but concentrations after higher injectable doses or nasal sprays have not been measured. In some hospital protocols, short-term (usually 24 hours) use of ketorolac injections after cesarean section has not been shown to be harmful to breastfed infants. However, due to the low production of colostrum, the amount of ketorolac ingested by the infant from colostrum is very low. Some evidence suggests that intravenous ketorolac as part of a multimodal analgesia regimen after cesarean section reduces the rate of mothers experiencing exclusive breastfeeding failure compared to patient-controlled intravenous morphine analgesia. Ketorolac has potent antiplatelet activity and may cause gastrointestinal bleeding. The manufacturer notes that ketorolac is contraindicated during lactation; therefore, other medications should be preferred during periods of high milk production, particularly in the first 24 to 72 hours postpartum, especially when nursing newborns or premature infants. Maternal use of ketorolac eye drops is not expected to have any adverse effects on breastfed infants. To significantly reduce the amount of medication that enters breast milk after using the eye drops, press the tear duct at the corner of the eye for 1 minute or longer, then wipe away any excess medication with absorbent tissue.
◉ Impact on Breastfed Infants
A randomized, double-blind study compared the effects of standard care on mothers who underwent cesarean section (n = 60) versus standard care plus multimodal analgesia (including a single intramuscular injection of 60 mg ketoroxyproline during fascial suturing) (n = 60). In the first month postpartum, there were no significant differences between the two groups in the incidence of neonatal growth abnormalities, feeding difficulties, neonatal sedation, or respiratory depression.
◉ Impact on Lactation and Breast Milk
A randomized, double-blind study compared the postpartum outcomes of mothers who underwent cesarean section (n = 60) versus standard care plus multimodal analgesia (including a single intramuscular injection of 60 mg ketoroxyproline during fascial suturing) (n = 60). In the first month postpartum, there were no significant differences in breastfeeding rates between the two groups (78% and 79%, respectively). In a study comparing standard postpartum care and enhanced recovery after cesarean section (ERAS), the ERAS regimen included a fixed dose of 15 mg ketodrolic acid intravenously every 6 hours for 24 hours postpartum, while the standard regimen included on-demand intravenous administration of 15 mg ketodrolic acid. Patients using the ERAS regimen (n = 58) had a higher rate of exclusive breastfeeding (67%) than those using the standard regimen (48%; n = 60). A retrospective study evaluated 1349 women who underwent cesarean section and received ketodrolic acid within 15 minutes of the end of surgery. Results showed no difference in pain control during the first 6 hours postoperatively or in the proportion of women breastfeeding at discharge.
A prospective cohort study compared postoperative pain control after cesarean section: (1) patient-controlled analgesia (PCA) with morphine for the first 12 hours postoperatively and ibuprofen administered at set times, followed by continued ibuprofen administration, with hydrocodone-acetaminophen added as needed; (2) a multimodal analgesia regimen including: (3) oral acetaminophen 1000 mg every 8 hours postoperatively; (4) intravenous ketorolac 30 mg, followed by 15 mg every 8 hours for 24 hours; (5) oral ibuprofen 600 mg every 8 hours for the remainder of postoperative time; opioids were used only when necessary. Among women who planned to exclusively breastfeed at admission, the proportion of women using formula before discharge was lower in the multimodal group than in the conventional group (9% vs. 12%).

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Protein binding
>99% of ketorolac is bound to plasma proteins.

[1]. Comparison of cyclooxygenase inhibitory activity and ocular anti-inflammatory effects of ketorolac tromethamine and bromfenac sodium. Curr Med Res Opin. 2006 Jun;22(6):1133-40.

[2]. Treatment with paracetamol, ketorolac or etoricoxib did not hinder alveolar bone healing: a histometric study in rats. J Appl Oral Sci. 2010 Dec;18(6):630-4.

[3]. Intrathecal ketorolac pretreatment reduced spinal cord ischemic injury in rats. Anesth Analg. 2005 Apr;100(4):1134-9.

[4]. Ketorolac salt is a newly discovered DDX3 inhibitor to treat oral cancer. Sci Rep. 2015 Apr 28;5:9982.

Pharmacodynamics
Ketoroxylic acid is a non-selective nonsteroidal anti-inflammatory drug (NSAID) that works by inhibiting cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), two enzymes normally responsible for converting arachidonic acid into prostaglandins. COX-1 enzyme has constitutive activity and is present in platelets, gastric mucosa, and vascular endothelial cells. COX-2 enzyme, on the other hand, has inducible activity, mediating inflammation, pain, and fever. Therefore, inhibition of COX-1 enzyme increases the risk of bleeding and gastric ulcers, while the desired anti-inflammatory and analgesic effects are associated with inhibition of COX-2 enzyme. Therefore, although ketoroxylic acid is effective in pain management, it should not be used long-term as this increases the risk of serious adverse reactions such as gastrointestinal bleeding, peptic ulcers, and perforation.

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1. Ketoroxylic acid is a nonsteroidal anti-inflammatory drug (NSAID). Its anti-inflammatory effect is mainly achieved by inhibiting the activity of COX-1 and COX-2, thereby reducing the synthesis of prostaglandins (such as PGE2) [1]
2. In a rat alveolar bone healing model, ketoroxylic acid (1 mg/kg, intraperitoneal injection, 7 days) did not affect the normal healing process of alveolar bone, which is of clinical significance for the application of ketoroxylic acid in post-extraction pain management [2]
3. The protective effect of intrathecal injection of ketoroxylic acid against spinal cord ischemia injury may be related to its antioxidant stress effect (reducing MDA production and increasing SOD activity) and inhibition of… neuronal necrosis [3]
4. DDX3 is a DEAD-box RNA helicase that is highly expressed in oral cancer and promotes cancer cell proliferation and survival by activating the AKT signaling pathway. Ketoroxylate inhibits the progression of oral cancer by specifically binding to DDX3, inhibiting its RNA helicase activity, and downregulating the AKT/Bcl-2 signaling pathway [4]

C15H13N1O3

255.27

255.089

74103-06-3

Ketorolac tromethamine salt;74103-07-4;(S)-Ketorolac;66635-92-5;(R)-Ketorolac;66635-93-6;Ketorolac-d5;1215767-66-0;Ketorolac hemicalcium;167105-81-9;Ketorolac-d4;1216451-53-4

3826

White to light yellow solid powder

1.3±0.1 g/cm3

493.2±40.0 °C at 760 mmHg

160-161°C

252.1±27.3 °C

0.0±1.3 mmHg at 25°C

1.659

2.08

59.3

1

3

3

19

376

0

OZWKMVRBQXNZKK-UHFFFAOYSA-N

InChI=1S/C15H13NO3/c17-14(10-4-2-1-3-5-10)13-7-6-12-11(15(18)19)8-9-16(12)13/h1-7,11H,8-9H2,(H,18,19)

5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid

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)

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。