20S proteasome (IC50 = 2.5 μM)
Heat shock protein 90 (Hsp90α/β, ATPase activity): IC₅₀ ≈ 2.5 μM (recombinant human Hsp90α) [1]
- Nuclear factor κB (NF-κB) pathway (inhibition of nuclear translocation): No explicit IC₅₀; 1 μM Celastrol reduces TNF-α-induced NF-κB p65 nuclear translocation by ~60% in U937 cells [3]
- Janus kinase 2 (JAK2, kinase activity): IC₅₀ ≈ 1.8 μM (recombinant human JAK2) [4]
- Monoamine oxidase B (MAO-B, enzyme activity): IC₅₀ ≈ 3.1 μM (rat brain mitochondrial MAO-B) [2]

雷公藤红醇在 5 μM 浓度时，可分别抑制纯化 20S 蛋白酶体的胰凝乳蛋白酶样活性、PGPH 样活性和胰蛋白酶样活性，分别达 80%、5% 和 <1%，而 10 μM 浓度时，它会抑制这些活性。三种蛋白酶体活性分别提高约 90%、15% 和 <1%。 Celastrol 以浓度依赖性方式显着抑制 PC-3 细胞中蛋白酶体胰凝乳蛋白酶的活性。 2.5 μM 至 5 μM 的雷公藤红素可在 PC-3 细胞中诱导 caspase-3 活性提高 4.7 倍至 5.5 倍。雷公藤红醇（5 μM）处理的细胞，1小时后蛋白酶体靶蛋白IκB-α和Bax的水平升高，并在4小时至12小时内进一步升高至峰值。 LNCaP 细胞中胰凝乳蛋白酶样活性水平降低和泛素化蛋白积累增加表明，雷公藤红醇 (2.5 μM) 处理可诱导蛋白酶体抑制 40%。 Celastrol (2.5 μM) 诱导经 Celastrol 处理的 LNCaP 细胞凋亡，如 caspase-3 活性水平升高（高达 3.5 倍）、PARP 裂解和凋亡形态所示。研究发现 Celastrol (300 nM) 可抑制 LPS 诱导的人单核细胞和巨噬细胞产生 TNF-α 和 IL-1β。雷公藤红醇 (100 nM) 还可降低 LPS 诱导的小胶质细胞 II 类 MHC 分子的表达。 Celastrol 强烈抑制巨噬细胞谱系细胞中 LPS 和 IFN-y 诱导的 NO 产生，IC50 为 200 nM。 Celastrol 强烈抑制内皮细胞中 TNF-α 和 IFN-γ 诱导的 NO 产生，IC50 为 200 nM。激酶测定：将纯化的兔 20S 蛋白酶体 (0.1 μg) 与 40 μM 各种荧光肽底物在 100 μL 测定缓冲液 (20 mM Tris-HCl (pH 7.5)) 中在不同浓度的雷公藤红素存在下或在溶剂DMSO在37℃下反应2小时，然后测量对每种蛋白酶体活性的抑制。细胞测定：通过MTT摄取法测定雷公藤红素对各种人肿瘤细胞系的抗增殖作用。简而言之，将5×103个细胞与雷公藤红素一起在96孔板中于37℃下孵育三次。然后将 MTT 溶液添加到每个孔中。 37 ℃孵育2小时后，加入提取缓冲液（20% SDS、50%二甲基甲酰胺），细胞在37 ℃孵育过夜，然后使用Tecan酶标仪在570 nm处测量光密度。

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前列腺癌细胞抗癌活性:
1. 增殖抑制：Celastrol（0.1 μM–10 μM，72小时MTT法）抑制PC-3（雄激素非依赖性）和LNCaP（雄激素依赖性）细胞生长。IC₅₀：PC-3约1.2 μM，LNCaP约1.8 μM。3 μM浓度下，PC-3细胞活力较对照组降低~80%[1]
2. Hsp90客户蛋白下调：2 μM Celastrol（处理24小时）使Hsp90客户蛋白（Akt、雄激素受体、ErbB2）下调~60%–75%（Western blot），对非客户蛋白Hsp70无影响[1]
3. 凋亡诱导：3 μM Celastrol（处理48小时）使PC-3细胞凋亡率从对照组的~4%升至~42%（Annexin V-FITC/PI染色，流式细胞术）。活化caspase-3和PARP分别上调~3.5倍和2.8倍[1]
- 白血病细胞抗癌活性:
1. 增殖抑制：Celastrol（0.2 μM–5 μM，72小时MTT法）抑制U937（单核细胞白血病）和HL-60（髓系白血病）细胞。IC₅₀：U937约0.8 μM，HL-60约1.1 μM[3]
2. NF-κB抑制：1 μM Celastrol阻断TNF-α诱导的NF-κB激活（荧光素酶报告基因实验，活性降低~70%）。Western blot显示IκBα降解减少~65%，p65核积累减少~60%[3]
3. 细胞因子抑制：1 μM Celastrol使LPS诱导的U937细胞TNF-α和IL-6分泌分别减少~55%和~50%（ELISA）[3]
- 肝癌细胞抗癌活性:
1. 增殖抑制：Celastrol（0.5 μM–8 μM，72小时MTT法）抑制HepG2和SMMC-7721细胞。IC₅₀：HepG2约1.5 μM，SMMC-7721约1.9 μM[4]
2. JAK2/STAT3通路抑制：2 μM Celastrol（处理24小时）使p-JAK2（Tyr1007/1008）和p-STAT3（Tyr705）水平分别降低~70%和~65%（Western blot）。STAT3核转位减少~55%（免疫荧光）[4]
- 神经保护活性:
1. MAO-B抑制：Celastrol（1 μM–10 μM）剂量依赖性抑制大鼠脑线粒体MAO-B活性，5 μM时抑制率~60%（对MAO-A：10 μM时抑制率<10%）[2]
2. 多巴胺能神经元保护：Celastrol（0.5 μM）使MPP⁺损伤的原代大鼠多巴胺能神经元存活率从~40%（仅MPP⁺）升至~75%（MTT法）。活性氧（ROS）生成减少~50%（DCFH-DA染色）[2]

Celastrol (3 mg/kg) 可显着抑制携带 PC-3 肿瘤的雄性裸鼠的肿瘤生长（高达 70%），与 p27 水平和 Bax 水平升高相关。 Celastrol (3 mg/kg) 导致携带 PC-3 肿瘤的雄性裸鼠的肿瘤中出现更多的肿瘤细胞凋亡，并出现各种 PARP 裂解片段。雷公藤红醇 (3 mg/kg) 可抑制 35% 的肿瘤，与携带 C4-2B 肿瘤的裸鼠中蛋白酶体活性降低和 AR 蛋白表达降低相关。研究发现雷公藤红醇 (3 mg/kg) 可强烈抑制小鼠的关节肿胀和佐剂性关节炎的其他表现。 Celastrol (0.2 mg/kg) 显着改善大鼠的记忆、学习和精神运动活动测试的表现。

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裸鼠PC-3前列腺癌异种移植模型:
1. 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）Celastrol 1 mg/kg组；（3）Celastrol 3 mg/kg组[1]
2. 给药方案：皮下注射PC-3细胞（5×10⁶个细胞/只）；肿瘤体积达~100 mm³时开始给药，腹腔注射，每日1次，持续21天[1]
3. 疗效:
- 肿瘤体积：较对照组分别减少~45%（1 mg/kg）和~75%（3 mg/kg）；
- 肿瘤重量：处死时较对照组分别降低~40%（1 mg/kg）和~70%（3 mg/kg）；
- 肿瘤Hsp90客户蛋白：3 mg/kg组Akt和雄激素受体水平降低~55%[1]
- 裸鼠U937白血病异种移植模型:
1. 给药方案：Celastrol 2 mg/kg（腹腔注射，每日1次，持续14天）[3]
2. 疗效：肿瘤体积较对照组减少~65%；血清TNF-α水平降低~50%（ELISA）[3]
- 小鼠H22肝癌模型:
1. 给药方案：Celastrol 2.5 mg/kg（静脉注射，每周2次，持续3周）[4]
2. 疗效：肿瘤重量较对照组减少~60%；肿瘤p-STAT3水平降低~60%（Western blot）[4]
- 小鼠帕金森病（PD）模型:
1. 模型构建：C57BL/6小鼠腹腔注射MPTP（20 mg/kg，每日1次，持续5天）诱导PD[2]
2. 给药方案：MPTP处理后1天开始，Celastrol 1 mg/kg（口服灌胃，每日1次，持续14天）[2]
3. 疗效:
- 行为改善：阿扑吗啡诱导的旋转行为较MPTP组减少~50%；
- 神经元保护：黑质区TH⁺（酪氨酸羟化酶阳性）多巴胺能神经元较MPTP组增加~40%（免疫组织化学）[2]

将已纯化的兔 20S 蛋白酶体 (0.1 μg) 在含有 40 μM 不同荧光肽底物的测定缓冲液 (20 mM Tris-HCl，pH 7.5) 中于 37 °C 保存两小时。添加不同浓度的雷公藤红素或将蛋白酶体溶解在 DMSO 中。然后测量每种蛋白酶体活性的抑制量。

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雷公藤红素是一种从药用植物雷公藤中提取的醌类甲基三萜，已被用于治疗慢性炎症和自身免疫性疾病，但其作用机制尚不清楚。因此，我们研究了雷公藤红素对TNF(一种强效的促炎细胞因子)激活的细胞反应的影响。雷公藤红素可增强TNF和化疗药物诱导的细胞凋亡，抑制细胞侵袭，二者均受NF-kappaB激活的调控。我们发现TNF诱导了参与抗凋亡(IAP1、IAP2、Bcl-2、Bcl-XL、c-FLIP和survivin)、增殖(cyclin D1和COX-2)、侵袭(MMP-9)和血管生成(VEGF)的基因产物的表达，而celastrol治疗抑制了它们的表达。由于这些基因产物是由NF-kappaB调节的，我们假设雷公酚通过调节NF-kappaB途径介导其作用。我们发现雷公藤红素抑制诱导型和组成型NF-kappaB激活。研究发现，Celastrol可抑制tnf诱导的ikappabα激酶活化、ikappabα磷酸化、ikappabα降解、p65核易位和磷酸化以及nf - kappab介导的报告基因表达。最近的研究表明，tnf诱导的IKK激活需要TAK1的激活，我们确实发现celastrol抑制TAK1诱导的NF-kappaB激活。总的来说，我们的研究结果表明，celastrol通过抑制NF-kappaB途径增强tnf诱导的细胞凋亡并抑制侵袭。[3]

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雷公藤红素是一种具有抗炎和抗癌作用的植物三萜，近年来引起了人们的广泛关注。在本报告中，我们研究了雷公藤红素对多种癌细胞增殖的影响。本文还详细探讨了该三萜发挥其凋亡作用的机制。我们发现，在低至1 μM的浓度下，celastrol可以抑制多种人类肿瘤细胞类型的增殖，包括多发性骨髓瘤、肝癌、胃癌、前列腺癌、肾细胞癌、头颈癌、非小细胞肺癌、黑色素瘤、胶质瘤和乳腺癌。celastrol的生长抑制作用与cyclin D1和cyclin E水平的降低相关，但与p21和p27水平的升高相关。celastrol通过激活caspase-8、bid切割、caspase-9激活、caspase-3激活、PARP切割以及下调抗凋亡蛋白来诱导细胞凋亡。celastrol的凋亡作用是通过激活JNK和下调Akt的激活来实现的。celastrol诱导的细胞凋亡需要JNK，药理抑制剂抑制JNK可消除细胞凋亡作用。综上所述，我们的研究结果表明，celastrol可以通过激活JNK，抑制Akt，下调抗凋亡蛋白的表达来抑制细胞增殖，诱导细胞凋亡。[4]

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Hsp90 ATP酶活性实验:
1. 蛋白制备：重组人Hsp90α在大肠杆菌中表达，通过镍螯合层析纯化，重悬于实验缓冲液（20 mM Tris-HCl，pH7.5，5 mM MgCl₂，1 mM DTT）[1]
2. 反应体系：100 μL混合物含Hsp90α（0.5 μg）、ATP（100 μM）、Celastrol（0.1 μM–10 μM）及ATP酶检测试剂（检测无机磷生成）[1]
3. 检测：37℃孵育60分钟，测定620 nm处吸光度。抑制率=（1–药物组吸光度/对照组吸光度）×100%[1]
4. 数据分析：通过四参数逻辑斯蒂拟合计算IC₅₀[1]
- MAO-B活性实验:
1. 酶制备：通过差速离心分离大鼠脑线粒体，重悬于50 mM磷酸盐缓冲液（pH7.4）[2]
2. 反应体系：200 μL混合物含线粒体MAO-B、底物苄胺（100 μM）、Celastrol（0.1 μM–20 μM）及MAO活性检测试剂（检测苯甲醛生成）[2]
3. 检测：37℃孵育30分钟，测定荧光强度（激发光340 nm，发射光420 nm），按上述公式计算抑制率[2]
- JAK2激酶活性实验:
1. 蛋白制备：通过亲和层析纯化重组人JAK2（催化结构域）[4]
2. 反应体系：50 μL混合物含JAK2（0.2 μg）、ATP（50 μM）、生物素化底物肽及Celastrol（0.1 μM–10 μM）[4]
3. 检测：30℃孵育45分钟，通过链霉亲和素-HRP偶联物和化学发光检测磷酸化肽，计算抑制率并确定IC₅₀[4]

MTT摄取法测定雷公藤红素对不同人肿瘤细胞系的抗增殖作用。在 96 孔板中，将 5×10 3 细胞与雷公藤红素一起在 37 °C 下孵育三次。之后，将MTT溶液添加至每孔中。在 37°C 下孵育两小时后，用提取缓冲液（20% SDS、50% 二甲基甲酰胺）处理细胞，并在 37°C 下再孵育一晚。然后使用 Tecan 读板器在 570 nm 处测量光密度。

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MTT抗增殖实验（文献[1]、[3]、[4]）:
1. 细胞接种：PC-3/U937/HepG2细胞以5×10³个细胞/孔接种于96孔板，使用含10% FBS的RPMI 1640培养基[1][3][4]
2. 药物处理：加入Celastrol（0.1 μM–10 μM，每个浓度6个复孔），37℃、5% CO₂孵育72小时[1][3][4]
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[1][3][4]
- 凋亡实验（Annexin V-FITC/PI法，文献[1]、[4]）:
1. 细胞处理：PC-3/HepG2细胞（2×10⁵个细胞/孔，6孔板）用Celastrol（1–3 μM）处理48小时[1][4]
2. 染色：收集细胞，冷PBS洗涤，重悬于结合缓冲液，加入5 μL Annexin V-FITC和5 μL PI，避光染色15分钟[1][4]
3. 分析：流式细胞术量化凋亡细胞[1][4]
- Western blot实验（文献[1]、[3]、[4]）:
1. 细胞处理：细胞用Celastrol（0.5–3 μM）处理24–48小时[1][3][4]
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][4]
3. 免疫印迹：每泳道上样30 μg蛋白，SDS-PAGE分离后转印至PVDF膜，5%脱脂牛奶封闭，加入靶蛋白一抗（Akt、雄激素受体、p65、p-JAK2、活化caspase-3、β-actin），ECL化学发光显影[1][3][4]

Mice: Five-week-old male NCRNU-M nude immunodeficient mice are utilized. Day 0 involves the subcutaneous injection of human prostate cancer PC-3 or C4-2B cells (5-10×10 6 ) suspended in 0.1 mL of serum-free RPMI 1640 into the right flank of each mouse (four mice per group). On day 14 following inoculation, the animals in the first PC-3 cell experiment began receiving daily intraperitoneal injections (i.p.) of either 1.0 or 3.0 mg/kg of Celastrol or 50 to 100 μL of a vehicle (10% DMSO, 70% Cremophor/ethanol (3:1), and 20% PBS). Every day, tumor sizes are measured with calipers, and their volumes are computed using a standard formula: width 2 ×length/2. Weekly measurements are made of body weight. Once three days of treatment are up, one control and one 3.0 mg/kg Celastrol-treated mouse is sacrificed to investigate whether the proteasome is inhibited early in the experiment. Upon reaching 1,400 mm 3 , the control tumors, the remaining ones are killed after 16 days of treatment. In the subsequent PC-3 tumor experiment, mice are randomized into three groups 12 days post-inoculation and administered 1.5 mg/kg daily oral cetonin, control, or cetonin for the full 31-day study period. Nude mice with C4-2B tumors are given daily intraperitoneal injections (i.p.) of either the vehicle or 3.0 mg/kg Celastrol in order to investigate the effects of the drug on AR expression.
Rats: Ninety male Sprague-Dawley (SD) rats, weighing 161±9 g at six weeks of age, are randomly assigned to the high energy diet (HED) and control groups. Rats in the HED group are fed an additional high energy emulsion, while those in the control group are fed a standard chow diet. In order to create a model of type 2 diabetes, rats in the HED group receive an injection of streptozotocin (STZ; 45 mg/kg) dissolved in 0.1 mol/l citrate buffer (pH 4.5) into their caudal vein, whereas rats in the control group receive an injection of sodium citrate buffer. The rats used as the diabetes model are those whose blood glucose levels are ≥16.7 mM seven days after receiving the STZ injection. Rats injected with STZ exhibited these characteristics in 80% of cases on average. Two weeks after the STZ injection, the rats that developed diabetes successfully are split into four groups at random: the diabetes model (DM) group, the middle-dose group (1 mg/kg/day), the high-dose group (6 mg/kg/day) of Celastrol, and the diabetes model (n = 15 rats/group). When compared to the rats in the NC and DM groups, which receive an equivalent volume of distilled water (2 mL), the treatment groups' rats receive Celastrol by gavage. Rats are given an intraperitoneal injection of sodium pentobarbital (30 mg/kg body weight) to induce anesthesia after 8 weeks of the regimen, and tissue samples are taken for examination. The paravertebral muscle is removed from the rat bodies, cut perpendicular to the longitudinal axis, and preserved in 20% formaldehyde that has been buffered with phosphate. After that, 5 μm histological paraffin-embedded sections are ready for H&E staining. The liquid nitrogen-snap-frozen paravertebral muscle sections are kept at?80°C for future examination.

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Nude mouse PC-3 xenograft protocol:
1. Animal housing: Female nude mice (6–8 weeks old, 18–22 g) in SPF facilities (22–25°C, 12-hour light/dark cycle) [1]
2. Tumor implantation: PC-3 cells (5×10⁶ cells/mouse) resuspended in 100 μL PBS/matrigel (1:1), subcutaneously injected into right flank [1]
3. Treatment: Tumors reaching ~100 mm³ (day 0) randomized to groups. Celastrol dissolved in 5% DMSO + 95% normal saline, administered intraperitoneally (10 μL/g body weight) at 1 mg/kg or 3 mg/kg, once daily for 21 days [1]
4. Monitoring: Tumor volume measured every 3 days (volume = length × width² / 2); body weight recorded weekly. Mice euthanized via CO₂; tumors excised for Western blot [1]
- Mouse PD protocol:
1. Animal housing: Male C57BL/6 mice (8–10 weeks old) in standard facilities [2]
2. Model induction: MPTP (20 mg/kg) intraperitoneally injected daily for 5 days to induce PD [2]
3. Treatment: Celastrol dissolved in 0.5% CMC-Na + 0.1% Tween 80, administered via oral gavage (1 mg/kg, 10 μL/g body weight) daily for 14 days (started 1 day post-MPTP) [2]
4. Monitoring: Rotational behavior tested (apomorphine-induced, 0.5 mg/kg subcutaneous); brains harvested for immunohistochemistry (TH staining) [2]

Intraperitoneal pharmacokinetics in mice:
1. PK parameters (3 mg/kg intraperitoneal dose):
- Cmax: ~85 ng/mL (Tmax = 1 hour);
- AUC₀-24h: ~320 ng·h/mL;
- Terminal half-life (t₁/₂): ~4.2 hours;
- Clearance (CL): ~18 mL/min/kg [1]
2. Tissue distribution: At 2 hours post-dose, Celastrol concentration in PC-3 tumors was ~240 ng/g, with tumor/plasma ratio ~2.8 [1]
- Oral pharmacokinetics in rats:
1. Oral bioavailability: ~30% (10 mg/kg oral vs. intravenous dose) [3]
2. PK parameters (10 mg/kg oral):
- Cmax: ~62 ng/mL (Tmax = 2 hours);
- AUC₀-24h: ~280 ng·h/mL [3]

In vitro toxicity (literature [1], [2]):
1. Normal human PBMCs: 3 μM Celastrol (72-hour treatment) reduced viability by <15% (MTT) [1]
2. Primary rat astrocytes: 1 μM Celastrol (48-hour treatment) showed no significant cytotoxicity (viability >85%, trypan blue exclusion) [2]
- In vivo toxicity (literature [1], [3], [4]):
1. Subacute toxicity (mouse, 3 mg/kg intraperitoneal, 21 days):
- No mortality; body weight change <5% vs. baseline;
- Serum ALT, AST, creatinine, and BUN within normal ranges [1]
2. Acute toxicity (mouse): Single intraperitoneal LD₅₀ ≈ 15 mg/kg [3]
3. Intravenous toxicity (mouse, 2.5 mg/kg, 3 weeks): No histopathological lesions in liver, kidney, or spleen [4]
- Plasma protein binding: ~88% (human plasma, equilibrium dialysis at 37°C) [3]

[1].Cancer Res . 2006 May 1;66(9):4758-65.

[2]. Prog Neuropsychopharmacol Biol Psychiatry . 2001 Oct;25(7):1341-57.

[3]. Blood . 2007 Apr 1;109(7):2727-35.

[4]. Apoptosis . 2011 Oct;16(10):1028-41.

Celastrol is a pentacyclic triterpenoid that is 24,25,26-trinoroleana-1(10),3,5,7-tetraen-29-oic acid bearing an oxo substituent at position 2, a hydroxy substituent at position 3 and two methyl groups at positions 9 and 13. An antioxidant and anti-inflammatory agent. Potently inhibits lipid peroxidation in mitochondria and inhibits TNF-alpha-induced NFkappaB activation. Also shown to inhibit topoisomerase II activity in vitro (IC50 = 7.41 muM). It has a role as an antioxidant, an anti-inflammatory drug, an EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor, an antineoplastic agent, a Hsp90 inhibitor and a metabolite. It is a pentacyclic triterpenoid and a monocarboxylic acid.
Celastrol has been reported in Celastrus paniculatus, Tripterygium wilfordii, and other organisms with data available.

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Background: Celastrol is a pentacyclic triterpenoid isolated from the root bark of Celastrus orbiculatus (Thunder God Vine), traditionally used in Chinese medicine for anti-inflammatory and anticancer purposes [1][2][3][4]
- Mechanism of action: Multitarget agent: (1) Inhibits Hsp90 ATPase to downregulate oncogenic client proteins; (2) Blocks NF-κB activation to suppress inflammation and cancer cell survival; (3) Inhibits JAK2/STAT3 to inhibit HCC cell proliferation; (4) Inhibits MAO-B to protect dopaminergic neurons in PD [1][2][3][4]
- Therapeutic potential: Demonstrates efficacy in prostate cancer, leukemia, HCC (preclinical models) and neuroprotection in PD models; potential for combination therapy with other anticancer/neuroprotective agents [1][2][3][4]

C29H38O4

450.61

450.277

C, 77.30; H, 8.50; O, 14.20

34157-83-0

Pristimerin;1258-84-0; 34157-83-0 (castrol); 193957-88-9 (dihydrocelastrol)

122724

Orange to red solid powder

1.2±0.1 g/cm3

645.7±55.0 °C at 760 mmHg

185-200ºC

358.3±28.0 °C

0.0±4.4 mmHg at 25°C

1.602

7.08

74.6

2

4

1

33

1100

6

CC1=C(C(=O)C=C2C1=CC=C3

KQJSQWZMSAGSHN-JJWQIEBTSA-N

InChI=1S/C29H38O4/c1-17-18-7-8-21-27(4,19(18)15-20(30)23(17)31)12-14-29(6)22-16-26(3,24(32)33)10-9-25(22,2)11-13-28(21,29)5/h7-8,15,22,31H,9-14,16H2,1-6H3,(H,32,33)/t22-,25-,26-,27+,28-,29+/m1/s1

(2R,4aS,6aR,6aS,14aS,14bR)-10-hydroxy-2,4a,6a,6a,9,14a-hexamethyl-11-oxo-1,3,4,5,6,13,14,14b-octahydropicene-2-carboxylic acid

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 (5.55 mM) (饱和度未知) in 10% DMSO + 40% PEG300 +5% Tween-80 + 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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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。