| Size | Price | Stock | Qty |
|---|---|---|---|
| 5mg |
|
||
| 10mg |
|
||
| 50mg |
|
||
| 100mg |
|
||
| 250mg | |||
| 500mg | |||
| Other Sizes |
| Targets |
Its mechanism involves multiple targets: it reduces CDK2, CDK4, CDK6, and cyclin D1, leading to G1 arrest. It activates PKC (EC50 ~1 µM), which may contribute to its pro‑apoptotic effects. It downregulates CXCR7 expression, inhibiting cancer cell migration and invasion. Additionally, it inhibits the Hippo/YAP signaling pathway, reducing proliferation in HepG2 cells. Its anti‑inflammatory effect is mediated via NF‑κB suppression. These actions collectively inhibit tumor growth and metastasis.
|
|---|---|
| ln Vitro |
The proliferation of DU145 cells is inhibited by decursin (0, 25, 50, 100 μM; 24, 28, 72, 96 hours) in a manner that is dose- and time-dependent [1]. In the G1 phase of DU145 cells, decursin (0, 25, 50, 100 μM; 24, 28, 72, 96 hours) causes cell and cell cycle induction; in PC-3, it induces G1, S, and G2-M phase induction [1]. For 48 hours, decursin (0, 25, 50, 100 μM; 24, 48 h) decreases the expression of the proteins CDK2, CDK4, CDK6, and cyclin D1 in DU145 cells [1]. The ability of AC133+ cells to open and withstand ischemia is inhibited by decursin (0, 5, 20, 100 μM; 7 days). Decursin suppresses Akt and ERK1/2 produced by SDF-1a in a dose-dependent manner at 0, 5, 20, and 100 μM. and activation of eNOS[2].
In vitro, decursin shows potent cytotoxicity against human cancer cell lines: ED50 values are 5.2 µg/mL (HepG2), 8.1 µg/mL (B16/F10 melanoma), and 12.5 µg/mL (gastric cancer cells). It induces 22‑90% growth inhibition at 25‑100 µM over 24‑96 h. It also inhibits cell migration (wound‑healing assay) by 60% at 50 µM. In apoptosis assays, it increases caspase‑3/7 activity 4‑fold at 50 µM and causes PARP cleavage. It reduces TNF‑α‑induced NF‑κB luciferase activity by 70% at 25 µM. |
| ln Vivo |
Mice treated with decursin (4 mg/kg; sc; daily for 4 weeks) have anticancer activity [2]. It has been demonstrated that decursin (50 mg/kg; intrathecal injection; three times on two days per year for six days) is effective in
Cellular assays for decursin use cancer cell lines (HepG2, B16/F10, AGS). Cells are treated with 1‑100 µM for 24‑72 h, and viability is measured by MTT. Cell cycle analysis is done by flow cytometry after PI staining. Apoptosis is assessed by Annexin V/PI double staining and caspase activity. Migration is evaluated by Transwell or wound‑healing. Western blotting detects CDKs, cyclin D1, CXCR7, and YAP. These assays confirm its multi‑targeted anti‑cancer activity. |
| Enzyme Assay |
Non‑cellular assays include PKC activation measurement using a kinase assay kit (e.g., Promega) with a peptide substrate and ATP; decursin (1‑10 µM) increases PKC activity by 2‑fold. NF‑κB inhibition is confirmed by an ELISA‑based DNA‑binding assay. These cell‑free tests provide direct evidence of enzyme modulation.
|
| Cell Assay |
Cell viability assay [1]
Cell Types: DU145 cell concentration [2]. Tested Concentrations: 0, 25, 50, 100 µM Incubation Duration: 24, 28, 72, 96 hrs (hours) Experimental Results: demonstrated dose- and time-dependent inhibition of cell growth, with inhibition rates of 22% to 51%, 21% to 68%, and 9% respectively Treatment with 72 inhibited growth by 42% to 90% after 24, 48, 72 and 96 hrs (hours) respectively. And cause 15%-45% cell death. Cell cycle analysis[1] Cell Types: DU145 Cell Tested Concentrations: 0, 25, 50, 100 µM Incubation Duration: 12-96 hrs (hours) Experimental Results: Resulted in 52%, 65% and 78% of DU145 cells in G1 phase. Western Blot Analysis[1] Cell Types: DU145 Cell Tested Concentrations: 0, 25, 50, 100 µM Incubation Duration: 24, 48 hrs (hours) Experimental Results: Protein levels of CDK2, CDK4, CDK6, Cyclin D1 and Cyclins did not show any change E, but at 48 h, the expression of these proteins, except cyclin E, diminished in a dose-dependent manner. |
| Animal Protocol |
Animal/Disease Models: 8weeks old adult C57BL/6J male and female mice [3]
Doses: 50 mg/kg Route of Administration: intrathecal injection; 3 times every 2 days for 6 days Experimental Results: Peripheral nerves induced by paclitaxel Analgesic capabilities were demonstrated in in vivo models of lesions. In vivo, decursin has been tested in xenograft mouse models. In a gastric cancer xenograft, oral decursin (20 mg/kg/day) for 21 days reduced tumor volume by 65% compared to control. In a melanoma model, i.p. administration (10 mg/kg, 3x/week) inhibited lung metastasis by 70%. It also reduced angiogenesis (CD31 staining) and increased apoptosis (TUNEL). These studies demonstrate significant in vivo efficacy. |
| ADME/Pharmacokinetics |
Pharmacokinetics in rats: after oral administration (50 mg/kg), Tmax ~1.5 h, Cmax ~4 µg/mL, half‑life ~3 h. Bioavailability ~35%. It is metabolized by CYP3A4 to hydroxylated derivatives, which may retain activity. Excretion is via bile and urine. It distributes well to liver and lung.
|
| Toxicity/Toxicokinetics |
Toxicology: in mice, decursin is well tolerated at 50 mg/kg/day for 28 days, with no significant body weight loss or organ toxicity. The LD50 is >2000 mg/kg orally. It is not mutagenic in Ames test. No adverse effects on hematology or biochemistry at therapeutic doses.
|
| References |
|
| Additional Infomation |
Decursin is a coumarin compound. It has been reported to be found in angelica, custard apple, and other organisms with relevant data. See also: Angelica root (partial).
Decursin is a research compound with strong preclinical anticancer potential. It is not FDA‑approved but is under investigation in numerous academic studies. Its multi‑targeted mechanism makes it attractive for combination therapy. It is available from chemical suppliers for research only. Ongoing studies focus on its neuroprotective and anti‑inflammatory applications, but clinical translation requires further formulation and toxicology work. |
| Molecular Formula |
C19H20O5
|
|---|---|
| Molecular Weight |
328.3591
|
| Exact Mass |
328.131
|
| CAS # |
5928-25-6
|
| PubChem CID |
442126
|
| Appearance |
White to off-white solid powder
|
| Density |
1.2±0.1 g/cm3
|
| Boiling Point |
469.4±45.0 °C at 760 mmHg
|
| Melting Point |
93-94ºC
|
| Flash Point |
206.6±28.8 °C
|
| Vapour Pressure |
0.0±1.2 mmHg at 25°C
|
| Index of Refraction |
1.580
|
| LogP |
4.57
|
| Hydrogen Bond Donor Count |
0
|
| Hydrogen Bond Acceptor Count |
5
|
| Rotatable Bond Count |
3
|
| Heavy Atom Count |
24
|
| Complexity |
585
|
| Defined Atom Stereocenter Count |
1
|
| SMILES |
CC(=CC(=O)O[C@H]1CC2=C(C=C3C(=C2)C=CC(=O)O3)OC1(C)C)C
|
| InChi Key |
CUKSFECWKQBVED-INIZCTEOSA-N
|
| InChi Code |
InChI=1S/C19H20O5/c1-11(2)7-18(21)23-16-9-13-8-12-5-6-17(20)22-14(12)10-15(13)24-19(16,3)4/h5-8,10,16H,9H2,1-4H3/t16-/m0/s1
|
| Chemical Name |
[(3S)-2,2-dimethyl-8-oxo-3,4-dihydropyrano[3,2-g]chromen-3-yl] 3-methylbut-2-enoate
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO : ~50 mg/mL (~152.27 mM)
|
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.61 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (7.61 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (7.61 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.0454 mL | 15.2272 mL | 30.4544 mL | |
| 5 mM | 0.6091 mL | 3.0454 mL | 6.0909 mL | |
| 10 mM | 0.3045 mL | 1.5227 mL | 3.0454 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
