货号:A909799
同义名:
前胡素
/ (+)-Decursin
Decursin ((+)-Decursin) 是一种有效的抗癌剂,具有细胞毒性和强效激活蛋白激酶 C (PKC) 的作用。Decursin 诱导细胞凋亡和 G1 期细胞周期停滞。Decursin 在 48 小时内减少 CDK2、CDK4、CDK6 和 cyclin D1 蛋白的表达。Decursin 抑制细胞增殖和迁移,具有抗肿瘤、抗炎和镇痛活性。


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| 产品名称 | VEGFR1 ↓ ↑ | VEGFR2 ↓ ↑ | VEGFR3 ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Motesanib Diphosphate |
++++
VEGFR1, IC50: 2 nM |
++++
VEGFR2, IC50: 3 nM VEGFR2/Flk1, IC50: 3 nM |
+++
VEGFR3, IC50: 6 nM |
RET,PDGFR | 97% | ||||||||||||||
| Tivozanib |
++
VEGFR1, IC50: 30 nM |
+++
VEGFR2, IC50: 6.5 nM |
++
VEGFR3, IC50: 15 nM |
99%+ | |||||||||||||||
| Brivanib |
+
VEGFR1, IC50: 380 nM |
++
Flk1, IC50: 25 nM VEGFR2, IC50: 25 nM |
99%+ | ||||||||||||||||
| Regorafenib |
+++
VEGFR1, IC50: 13 nM |
+++
VEGFR2, IC50: 4.2 nM |
+
VEGFR3, IC50: 46 nM |
RET | 98% | ||||||||||||||
| Pazopanib |
+++
VEGFR1, IC50: 10 nM |
++
VEGFR2, IC50: 30 nM |
+
VEGFR3, IC50: 47 nM |
c-Kit,PDGFR,FGFR | 99% | ||||||||||||||
| Sitravatinib |
+++
VEGFR1 (FLT1), IC50: 6 nM |
+++
VEGFR2 (KDR), IC50: 5 nM |
++++
VEGFR3 (FLT4), IC50: 2 nM |
99%+ | |||||||||||||||
| Foretinib |
+++
VEGFR1/FLT1, IC50: 6.8 nM |
++++
KDR, IC50: 0.86 nM |
++++
VEGFR3/FLT4, IC50: 2.8 nM |
Tie-2 | 99%+ | ||||||||||||||
| MGCD-265 analog |
++++
VEGFR1, IC50: 3 nM |
++++
VEGFR2, IC50: 3 nM |
++++
VEGFR3, IC50: 4 nM |
Tie-2 | 99%+ | ||||||||||||||
| Lactate |
+++
VEGFR1/FLT1, IC50: 10 nM |
+++
VEGFR2/Flk1, IC50: 13 nM |
+++
VEGFR3/FLT4, IC50: 8 nM |
c-Kit,FLT3 | 85% | ||||||||||||||
| AEE788 |
+
FLT1, IC50: 59 nM |
+
KDR, IC50: 77 nM |
EGFR | 98+% | |||||||||||||||
| Linifanib |
++++
VEGFR1/FLT1, IC50: 3 nM |
++++
VEGFR2/KDR, IC50: 4 nM |
+
VEGFR3/FLT4, IC50: 190 nM |
FLT3 | 99%+ | ||||||||||||||
| Vatalanib 2HCl |
+
VEGFR1/FLT1, IC50: 77 nM |
++
VEGFR2/Flk1, IC50: 270 nM VEGFR2/KDR, IC50: 37 nM |
+
VEGFR3/FLT4, IC50: 660 nM |
c-Kit,c-Fms/CSF1R | 99%+ | ||||||||||||||
| Axitinib |
++++
VEGFR1/FLT1, IC50: 0.1 nM |
++++
VEGFR2/Flk1, IC50: 0.18 nM VEGFR2/KDR, IC50: 0.2 nM |
98% | ||||||||||||||||
| Dovitinib |
+++
VEGFR1/FLT1, IC50: 10 nM |
+++
VEGFR2/Flk1, IC50: 13 nM |
+++
VEGFR3/FLT4, IC50: 8 nM |
c-Kit,FLT3 | 99%+ | ||||||||||||||
| ZM 306416 |
+
VEGFR1, IC50: 0.33 μM |
Src | 99%+ | ||||||||||||||||
| KRN-633 |
+
VEGFR1, IC50: 170 nM |
+
VEGFR2, IC50: 160 nM |
+
VEGFR3, IC50: 125 nM |
c-Kit,BTK | 98% | ||||||||||||||
| OSI-930 |
+++
FLT1, IC50: 8 nM |
+++
KDR, IC50: 9 nM |
99%+ | ||||||||||||||||
| Lenvatinib |
++
VEGFR1/FLT1, IC50: 22 nM |
++++
VEGFR2/KDR, IC50: 4.0 nM |
+++
VEGFR3/FLT4, IC50: 5.2 nM |
98% | |||||||||||||||
| NVP-BAW2881 |
+
hVEGFR1, IC50: 820 nM |
+++
hVEGFR2, IC50: 9 nM mVEGF2, IC50: 165 nM |
+
hVEGFR3, IC50: 420 nM |
99% | |||||||||||||||
| Cediranib |
+++
VEGFR1/FLT1, IC50: 5 nM |
++++
VEGFR2/KDR, IC50: 0.5 nM |
c-Kit | 99%+ | |||||||||||||||
| Nintedanib |
++
VEGFR1, IC50: 34 nM |
+++
VEGFR2, IC50: 13 nM |
+++
VEGFR3, IC50: 13 nM |
FLT3 | 99+% | ||||||||||||||
| BMS-794833 |
++
VEGFR2, IC50: 15 nM |
99%+ | |||||||||||||||||
| SKLB1002 |
++
VEGFR2, IC50: 32 nM |
99% | |||||||||||||||||
| Cabozantinib S-malate |
++++
VEGFR2/KDR, IC50: 0.035 nM |
99+% | |||||||||||||||||
| Ki8751 |
++++
VEGFR2, IC50: 0.9 nM |
c-Kit | 99% | ||||||||||||||||
| SU 5402 |
++
VEGFR2, IC50: 20 nM |
98% | |||||||||||||||||
| Apatinib mesylate |
++++
VEGFR2, IC50: 1 nM |
RET | 98+% | ||||||||||||||||
| Ponatinib |
++++
VEGFR2, IC50: 1.5 nM |
98% | |||||||||||||||||
| LY2874455 |
+++
VEGFR2, IC50: 7 nM |
99%+ | |||||||||||||||||
| ZM323881 HCl |
++++
VEGFR2, IC50: <2 nM |
98% | |||||||||||||||||
| AZD2932 |
+++
VEGFR-2, IC50: 8 nM |
c-Kit | 99% | ||||||||||||||||
| Cabozantinib |
++++
VEGFR2/KDR, IC50: 0.035 nM |
98% | |||||||||||||||||
| Sorafenib |
++
VEGFR2, IC50: 90 nM VEGFR2/Flk1, IC50: 90 nM |
99% | |||||||||||||||||
| CYC-116 |
++
VEGFR2, Ki: 44 nM |
FLT3 | 99%+ | ||||||||||||||||
| Golvatinib |
++
VEGFR2, IC50: 16 nM |
99%+ | |||||||||||||||||
| Sunitinib |
+
VEGFR2 , IC50: 80 nM |
FLT3 | 98% | ||||||||||||||||
| RAF265 |
++
VEGFR2, EC50: 30 nM |
99%+ | |||||||||||||||||
| PD173074 | 99%+ | ||||||||||||||||||
| BFH772 |
++++
VEGFR2, IC50: 3 nM |
98% | |||||||||||||||||
| Semaxinib |
+
VEGFR2/Flk1, IC50: 1.23 μM |
98% | |||||||||||||||||
| Vandetanib |
++
VEGFR2, IC50: 40 nM |
+
VEGFR3, IC50: 110 nM |
EGFR | 99% | |||||||||||||||
| SAR131675 |
++
VEGFR3, IC50: 23 nM |
99%+ | |||||||||||||||||
| ENMD-2076 |
+
VEGFR2/KDR, IC50: 58.2 nM |
++
VEGFR3/FLT4, IC50: 15.9 nM |
RET,FLT3 | 98% | |||||||||||||||
| Telatinib |
+++
VEGFR2, IC50: 6 nM |
++++
VEGFR3, IC50: 4 nM |
c-Kit | 99%+ | |||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 产品名称 | CXCR1 ↓ ↑ | CXCR2 ↓ ↑ | CXCR4 ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Reparixin | ✔ | 99%+ | |||||||||||||||||
| SB225002 |
+++
CXCR2, IC50: 22 nM |
99%+ | |||||||||||||||||
| Plerixafor |
++
CXCR4, IC50: 44 nM |
99% | |||||||||||||||||
| AMD 3465 6HBr | ✔ | 98% | |||||||||||||||||
| WZ811 |
++++
CXCR4, EC50: 0.3 nM |
99% | |||||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 产品名称 | PKC ↓ ↑ | PKCα ↓ ↑ | PKCβ ↓ ↑ | PKCγ ↓ ↑ | PKCδ ↓ ↑ | PKCε ↓ ↑ | PKCζ ↓ ↑ | PKCη ↓ ↑ | PKCθ ↓ ↑ | 其他靶点 | 纯度 | ||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Daphnetin |
+
PKC, IC50: 25.01 μM |
EGFR,PKA | 95% | ||||||||||||||||
| Dequalinium Chloride | 99%+ | ||||||||||||||||||
| Quercetin | ✔ | Sirtuin,Src | 95% | ||||||||||||||||
| Myricetrin | ✔ | 96% | |||||||||||||||||
| Go 6983 |
+++
PKCα, IC50: 7 nM |
+++
PKCβ, IC50: 7 nM |
+++
PKCγ, IC50: 6 nM |
+++
PKCδ, IC50: 10 nM |
++
PKCζ, IC50: 60 nM |
99%+ | |||||||||||||
| Go6976 |
+++
PKC, IC50: 7.9 nM |
++++
PKCα, IC50: 2.3 nM |
+++
PKCβ1, IC50: 6.2 nM |
FLT3 | 99%+ | ||||||||||||||
| Bisindolylmaleimide I |
+++
PKCα, IC50: 20 nM |
+++
PKCβ2, IC50: 16 nM PKCβ1, IC50: 17 nM |
+++
PKCγ, IC50: 20 nM |
99%+ | |||||||||||||||
| Lawsone methyl ether | ✔ | 99% | |||||||||||||||||
| Sotrastaurin |
++++
PKCα, Ki: 0.95 nM |
++++
PKCβ1, Ki: 0.64 nM |
++++
PKCδ, Ki: 2.1 nM |
++++
PKCε, Ki: 3.2 nM |
++++
PKCη, Ki: 1.8 nM |
++++
PKCθ, Ki: 0.22 nM |
99%+ | ||||||||||||
| Enzastaurin |
++
PKCα, IC50: 39 nM |
+++
PKCβ, IC50: 6 nM |
+
PKCγ, IC50: 83 nM |
+
PKCε, IC50: 110 nM |
98% | ||||||||||||||
| Midostaurin |
++
PKCα, IC50: 22 nM |
++
PKCβ2, IC50: 31 nM PKCβ1, IC50: 30 nM |
++
PKCγ, IC50: 24 nM |
+
PKCδ, IC50: 330 nM |
+
PKCε, IC50: 1.25 μM |
+
PKCη, IC50: 160 nM |
99% | ||||||||||||
| Ro 31-8220 mesylate |
++++
PKCα, IC50: 5 nM |
+++
PKCβ2, IC50: 14 nM PKCβ1, IC50: 24 nM |
++
PKCγ, IC50: 27 nM |
++
PKCε, IC50: 24 nM |
99%+ | ||||||||||||||
| Staurosporine |
++++
PKCα, IC50: 2 nM |
++++
PKCγ, IC50: 5 nM |
+++
PKCδ, IC50: 20 nM |
++
PKCε, IC50: 73 nM |
++++
PKCη, IC50: 4 nM |
99%+ | |||||||||||||
| Ruboxistaurin HCl |
+
PKCα, IC50: 0.36 μM |
++++
PKCβ2, IC50: 5.9 nM PKCβ1, IC50: 4.7 nM |
+
PKCγ, IC50: 0.3 μM |
+
PKCδ, IC50: 0.25 μM |
++
PKCη, IC50: 0.052 μM |
99%+ | |||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 产品名称 | ALK1 ↓ ↑ | ALK2 ↓ ↑ | ALK3 ↓ ↑ | ALK4 ↓ ↑ | ALK6 ↓ ↑ | Smad3 ↓ ↑ | TGF-β ↓ ↑ | TGFβRI/ALK5 ↓ ↑ | TGFβRII ↓ ↑ | 其他靶点 | 纯度 | ||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| LDN193189 |
++++
ALK1, IC50: 0.8 nM |
++++
ALK2, IC50: 0.8 nM |
+++
ALK3, IC50: 5.3 nM |
+++
ALK6, IC50: 16.7 nM |
99%+ | ||||||||||||||
| LDN-212854 |
++++
ALK1, IC50: 2.4 nM |
++++
ALK2, IC50: 1.3 nM |
+
ALK3, IC50: 85.8 nM |
+
ALK4, IC50: 2133 nM |
+
ALK5, IC50: 9276 nM |
99%+ | |||||||||||||
| ML347 |
++
ALK1, IC50: 46 nM |
++
ALK2, IC50: 32 nM |
98% | ||||||||||||||||
| K02288 |
++++
ALK1, IC50: 1.8 nM |
++++
ALK2, IC50: 1.1 nM |
++
ALK3, IC50: 34.4 nM |
+++
ALK6, IC50: 6.4 nM |
99%+ | ||||||||||||||
| LDN-193189 2HCl |
++++
ALK1, IC50: 0.8 nM |
++++
ALK2, IC50: 0.8 nM |
+++
ALK3, IC50: 5.3 nM |
+++
ALK6, IC50: 16.7 nM |
99% | ||||||||||||||
| LDN-214117 |
++
ALK2, IC50: 24 nM |
98% | |||||||||||||||||
| DMH-1 |
+
ALK2, IC50: 107.9 nM |
99%+ | |||||||||||||||||
| SB-505124 |
+
ALK4, IC50: 129 nM |
++
ALK5, IC50: 47 nM |
99%+ | ||||||||||||||||
| Vactosertib |
+++
ALK4, IC50: 13 nM |
+++
ALK5, IC50: 11 nM |
99%+ | ||||||||||||||||
| Alantolactone | ✔ | 98% | |||||||||||||||||
| (E/Z)-SIS3 free base | ✔ | 97% | |||||||||||||||||
| Pirfenidone | ✔ | 98% | |||||||||||||||||
| Hesperetin | ✔ | 97% | |||||||||||||||||
| RepSox |
++++
TGFβR1(ALK5), IC50: 4 nM |
98% | |||||||||||||||||
| GW788388 |
+++
ALK5, IC50: 18 nM |
98% | |||||||||||||||||
| LY364947 |
++
TGFβRI, IC50: 59 nM |
+
TGFβRII, IC50: 0.4 μM |
98% | ||||||||||||||||
| SD-208 |
++
TGF-βRI (ALK5), IC50: 48 nM |
99% | |||||||||||||||||
| SB-525334 |
+++
TGFβR1(ALK5), IC50: 14.3 nM |
99%+ | |||||||||||||||||
| LY2109761 |
++
TβRI, Ki: 38 nM |
+
TβRII, Ki: 300 nM |
99%+ | ||||||||||||||||
| Galunisertib |
++
TβRI, IC50: 56 nM |
98% | |||||||||||||||||
| SB 431542 |
+
ALK5, IC50: 94 nM |
99%+ | |||||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 描述 | Decursin, identified as (+)-Decursin, serves as a potent anti-tumor agent with additional cytotoxic properties and the ability to activate protein kinase C significantly. It triggers apoptosis and causes cell cycle arrest in the G1 phase while reducing the expression of CDK2, CDK4, CDK6, and cyclin D1 proteins over 48 hours. Beyond its anti-tumor capacity, Decursin also displays anti-inflammatory and analgesic effects, inhibiting cell proliferation and migration[1].[2].[3].[4]. |
| 体内研究 | In in vivo models, Decursin demonstrates anti-tumor activity at a dosage of 4 mg/kg, administered subcutaneously daily for four weeks in mice[2]. Additionally, at a dosage of 50 mg/kg via intrathecal injection three times at two-day intervals over six days, it exhibits analgesic properties in a mouse model of paclitaxel-induced peripheral neuropathy[3]. |
| 体外研究 | In DU145 cells, Decursin exhibits a dose- and time-dependent inhibition of cell growth when administered in concentrations of 0, 25, 50, and 100 μM over periods of 24, 48, 72, and 96 hours[1]. Decursin not only induces apoptosis and G1 phase cell cycle arrest in DU145 cells but also leads to G1, S, and G2-M phase arrests in PC-3 cells[1]. Additionally, at concentrations of 0, 25, 50, and 100 μM over 24 and 48 hours, Decursin significantly decreases the levels of CDK2, CDK4, CDK6, and cyclin D1 protein in DU145 cells[1]. Further studies reveal that Decursin, at concentrations of 0, 5, 20, and 100 μM over seven days, inhibits both the proliferation and differentiation abilities of AC133+ cells[2]. It also dose-dependently blocks SDF-1α-induced activation of Akt, ERK1/2, and eNOS[2]. |
| Concentration | Treated Time | Description | References | |
| BEAS-2B | 60 μM | 1 h | To evaluate the effect of Decursin on ROS generation in normal cells, results showed that Decursin did not significantly induce ROS generation in normal cells | Br J Pharmacol. 2016 Mar;173(6):1033-44 |
| Calu-1 | 150 μM | 24 h | To evaluate the effect of Decursin on cell viability, results showed that Decursin significantly reduced the viability of NSCLC cells | Br J Pharmacol. 2016 Mar;173(6):1033-44 |
| H1299 | 150 μM | 24 h | To evaluate the effect of Decursin on cell viability, results showed that Decursin significantly reduced the viability of NSCLC cells | Br J Pharmacol. 2016 Mar;173(6):1033-44 |
| H596 | 150 μM | 24 h | To evaluate the effect of Decursin on cell viability, results showed that Decursin significantly reduced the viability of NSCLC cells | Br J Pharmacol. 2016 Mar;173(6):1033-44 |
| A549 | 150 μM | 24 h | To evaluate the effect of Decursin on cell viability, results showed that Decursin significantly reduced the viability of NSCLC cells | Br J Pharmacol. 2016 Mar;173(6):1033-44 |
| HT22 cells | 25 and 50 µM | 6 h | Evaluate the effect of Decursin on HO-1 expression in HT22 cells, results showed Decursin significantly increased HO-1 expression levels. | Antioxidants (Basel). 2023 Aug 21;12(8):1651 |
| HT22 cells | 25 and 50 µM | 8 h | Evaluate the effect of Decursin on glutamate-induced ROS accumulation in HT22 cells, results showed Decursin significantly reduced ROS accumulation. | Antioxidants (Basel). 2023 Aug 21;12(8):1651 |
| HT22 cells | 25 µM | 12 h | Evaluate the protective effect of Decursin on glutamate-induced chromatin condensation in HT22 cells, results showed Decursin significantly reduced chromatin condensation. | Antioxidants (Basel). 2023 Aug 21;12(8):1651 |
| HT22 cells | 12.5 and 25 µM | 24 h | Evaluate the protective effect of Decursin on glutamate-induced HT22 cell death, results showed Decursin significantly improved cell viability. | Antioxidants (Basel). 2023 Aug 21;12(8):1651 |
| F11 cells | 2 μM | 12 h | Decursin significantly increased the number and length of neurites in F11 cells, promoting neuronal regeneration. | Cells. 2021 Mar 4;10(3):547 |
| F11 cells | 0.5 and 1 μM | 30 seconds | Decursin significantly inhibited the rapid elevation of intracellular Ca2+ levels induced by capsaicin in a concentration-dependent manner. | Cells. 2021 Mar 4;10(3):547 |
| HCT-8 colorectal cancer cells | 3.125, 6.25, 12.5, 25, 50, 100, 200 µM | 24, 48, 72 h | To evaluate the effect of Decursin on the growth of HCT-8 cells, results showed that Decursin inhibited cell viability in a dose- and time-dependent manner. | Int J Mol Sci. 2024 Sep 14;25(18):9939 |
| HCT-116 colorectal cancer cells | 3.125, 6.25, 12.5, 25, 50, 100, 200 µM | 24, 48, 72 h | To evaluate the effect of Decursin on the growth of HCT-116 cells, results showed that Decursin inhibited cell viability in a dose- and time-dependent manner. | Int J Mol Sci. 2024 Sep 14;25(18):9939 |
| Peripheral blood lymphocytes (PBL) | 80 μM | 24 h | To evaluate the cytotoxic effect of Decursin on PBL, results showed no cytotoxicity at concentrations up to 80 μM. | Cancer Lett. 2010 Dec 8;298(2):212-21 |
| U937 cells | 20, 80 μM | 24 h | To evaluate the cytotoxic effect of Decursin on U937 cells, results showed cytotoxicity starting at 20 μM, becoming prominent at 80 μM. | Cancer Lett. 2010 Dec 8;298(2):212-21 |
| HL-60 cells | 80 μM | 24 h | To evaluate the cytotoxic effect of Decursin on HL-60 cells, results showed an apoptotic effect at 80 μM. | Cancer Lett. 2010 Dec 8;298(2):212-21 |
| KBM-5 cells | 10, 20, 40, 80 μM | 24 h | To evaluate the cytotoxic effect of Decursin on KBM-5 cells, results showed that Decursin started to be cytotoxic at 10 μM and exhibited dose-dependent cytotoxicity. | Cancer Lett. 2010 Dec 8;298(2):212-21 |
| Administration | Dosage | Frequency | Description | References | ||
| C57BL/6J mice | Paclitaxel-induced neuropathic pain model | Intrathecal injection | 50 mg/kg | Every 2 days, 3 times in total, lasting 6 days | Decursin significantly alleviated mechanical allodynia in paclitaxel-induced neuropathic pain mice, and the effect was more prolonged with increased injection frequency. | Cells. 2021 Mar 4;10(3):547 |
| BALB/c nude mice | HCT-116 and HCT-8 colorectal cancer cell subcutaneous xenograft model | Intraperitoneal injection | 10 mg/kg | Twice weekly for 14 days | To evaluate the effect of Decursin on the growth of HCT-116 and HCT-8 xenografts, results showed that Decursin significantly suppressed tumor growth without causing host toxicity. | Int J Mol Sci. 2024 Sep 14;25(18):9939 |
| Nude mice | Subcutaneous xenograft model | Intraperitoneal injection | 10 mg/kg | On days 1, 3, 5, and 7 | To validate the anti-tumor efficacy of Decursin in vivo. The results showed that Decursin significantly inhibited tumor growth and no significant systemic toxicity was observed. | Int J Mol Sci. 2025 Jun 4;26(11):5391 |
| 计算器 | ||||
| 存储液制备 | ![]() |
1mg | 5mg | 10mg |
|
1 mM 5 mM 10 mM |
3.05mL 0.61mL 0.30mL |
15.23mL 3.05mL 1.52mL |
30.45mL 6.09mL 3.05mL |
|
| CAS号 | 5928-25-6 |
| 分子式 | C19H20O5 |
| 分子量 | 328.36 |
| SMILES Code | CC(C)=CC(O[C@@H]1C(C)(C)OC2=C(C=C(C=CC(O3)=O)C3=C2)C1)=O |
| MDL No. | MFCD00272154 |
| 别名 | 前胡素 ;(+)-Decursin |
| 运输 | 蓝冰 |
| 存储条件 |
In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Sealed in dry, store in freezer, under -20°C |
| 溶解方案 |
DMSO: 50 mg/mL(152.27 mM),配合低频超声助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO 以下溶解方案都请先按照体外实验的方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议现用现配,当天使用; 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶
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