| Size | Price | |
|---|---|---|
| 500mg | ||
| 1g | ||
| Other Sizes |
| ln Vitro |
6-Methoxydihydrosandriline (0.15625-10 μM; 24 hours) hydrochloride inhibited the viability of A549 and H1299 non-small cell lung cancer (NSCLC) cells in a dose-dependent manner, with IC50 values of 2.154 μM and 2.586 μM after 24 hours of treatment, respectively[1]. Treatment with 6-methoxydihydrosandriline (0.5-2 μM; 24 hours) hydrochloride at a concentration of 2 μM for 24 hours induced G2/M phase arrest in A549 and H1299 NSCLC cells, and at lower concentrations induced G1 phase arrest in H1299 cells[1]. Treatment with 6-methoxydihydrosandronate (0.5-2 μM; 24 h) hydrochloride for 24 hours downregulated the expression of cell cycle-related proteins Cdc25C, p-Cdc25C, cyclin B1, and Cdc2 in A549 and H1299 non-small cell lung cancer (NSCLC) cells [1]. Treatment with 6-methoxydihydrosandronate (0.5-2 μM; 24 h) hydrochloride for 24 hours dose-dependently activated the caspase cascade and induced PARP lysis in A549 and H1299 NSCLC cells, thereby promoting apoptosis [1]. 6-Methoxydihydrosandriline (0.5-2 μM; 24 hours) hydrochloride, after treatment for 24 hours, dose-dependently inhibited the Akt/mTOR signaling pathway in A549 and H1299 non-small cell lung cancer (NSCLC) cells by reducing the phosphorylation levels of Akt and p70S6K and the total protein level [1]. 6-Methoxydihydrosandriline (0.5-2 μM; 24 hours) hydrochloride, after treatment for 24 hours, dose-dependently blocked the YAP/TAZ oncogenic signaling pathway in A549 and H1299 NSCLC cells by reducing the expression of YAP, TAZ and survivin and increasing the phosphorylation level of LATS1/2 [1]. 6-Methoxydihydrosandriline (0.5-2 μM; 24 h) hydrochloride induced apoptosis in A549 and H1299 NSCLC cells in a dose-dependent manner after 24 hours of treatment [1]. 6-Methoxydihydrosandriline (0.5-2 μM; 12 h) hydrochloride increased the level of reactive oxygen species (ROS) in A549 and H1299 non-small cell lung cancer (NSCLC) cells in a dose-dependent manner after 12 hours of treatment [1]. 6-Methoxydihydrosandriline (0.5-2 μM; 24 h) hydrochloride activated the IRE1/JNK signaling pathway in A549 and H1299 NSCLC cells in a dose-dependent manner after 24 hours of treatment [1]. 6-Methoxydihydrosandricaline hydrochloride (0.125-8 μM; 24 hours) decreased the viability of HepG2 and Huh7 cells in a dose-dependent manner after 24 hours of treatment, with IC50 values of 2.83 μM and 3.46 μM, respectively [2]. 6-Methoxydihydrosandricaline hydrochloride (6-MS) (1-2 μM; 12 hours) increased the production of ROS in HepG2 and Huh7 cells in a dose-dependent manner, and this phenomenon was observed after 12 hours of treatment [2]. 6-Methoxydihydrosandricaline hydrochloride (0.5-2 μM; 24 hours) inhibited the EGFR/Akt signaling pathway in HepG2 and Huh7 cells in a dose-dependent manner, manifested as a decrease in EGFR expression and Akt phosphorylation levels, and this phenomenon was observed after 24 hours of treatment [2]. 6-Methoxydihydrosandriline hydrochloride (0.5–2 μM; 24 h) can activate the JNK and p38MAPK pathways in HepG2 and Huh7 cells, with JNK activation being essential for 6-MS-induced PARP lysis (a marker of apoptosis) [2]. 6-Methoxydihydrosandriline hydrochloride (0.5–2 μM; 24 h) upregulated the expression of DR4 and DR5 in HepG2 and Huh7 cells in a dose-dependent manner after 24 hours of treatment, and the upregulation of DR5 was essential for the 6-Methoxydihydrosandriline hydrochloride-mediated TRAIL-induced apoptosis sensitization [2]. 6-Methoxydihydrosandricaline hydrochloride (0-1.5 μM; 12 h) effectively inhibited the viability of HLE and HCCLM3 hepatocellular carcinoma cells after 12 hours, with IC50 values of 1.129 μM and 1.308 μM, respectively, and showed low cytotoxicity to normal LX-2 hepatic stellate cells [3]. Treatment with 6-methoxydihydrosandricaline hydrochloride (1 μM (HLE), 1.5 μM (HCCLM3); 12 h) for 12 hours induced hepatocellular carcinoma cell death, and this effect was mediated by ferroptosis, which could be reversed by ferroptosis inhibitors [3]. Treatment with 6-methoxydihydrosandricaline hydrochloride (1 μM (HLE), 1.5 μM (HCCLM3); 6 h) for 6 hours downregulated the expression of GPX4 in hepatocellular carcinoma cells at the transcriptional level [3]. 6-Methoxydihydrosandricaline hydrochloride (1-50 μM; 24 hours) selectively inhibited the viability of human A375 melanoma cells, while having no significant effect on normal NHDF cells, with an IC50 value of 2.85 μM after 24 hours [4]. 6-Methoxydihydrosandricaline hydrochloride (0-32 μM; 24 hours) significantly reduced the viability of MCF-7 breast cancer cells in a time- and dose-dependent manner, with an IC50 value of 4.21 μM after 24 hours [5]. 6-Methoxydihydrosandricaline hydrochloride (2-4 μM; 6-24 hours) induced apoptosis in MCF-7 breast cancer cells by upregulating pro-apoptotic proteins and downregulating anti-apoptotic proteins, induced autophagy by upregulating autophagy-related proteins, and inhibited the PI3K/AKT/mTOR pathway by reducing the phosphorylation level of key pathway proteins [5]. 6-Methoxydihydrosandriline hydrochloride can downregulate the expression of EFG1, CDC35, RAS1 and TPK2, which are key components of the cAMP pathway. In addition, 6-Methoxydihydrosandriline hydrochloride alters the membrane permeability of Candida albicans, leading to the accumulation of reactive oxygen species and consequently cell death [6].
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| ln Vivo |
6-Methoxydihydrosandronate (5 mg/kg; intraperitoneal injection; daily; 14 days) hydrochloride reduced tumor volume and weight in a Caov-3 mouse xenograft model of ovarian cancer [7].
|
| Cell Assay |
Cell viability assay [1]
Cell Types: A549, H1299 non-small cell lung cancer (NSCLC) cells Tested Concentrations: 0.15625 μM, 0.3125 μM, 0.625 μM, 1.25 μM, 2.5 μM, 5 μM, 10 μM Incubation Duration: 24 hours Experimental Results: Both cell lines showed a dose-dependent decrease in cell viability. The IC50 value for A549 cells was 2.154 μM, and the IC50 value for H1299 cells was 2.586 μM. Cell cycle analysis [1] Cell Types: A549, H1299 non-small cell lung cancer (NSCLC) cells Tested Concentrations: 0.5 μM, 1 μM, 2 μM Incubation Duration: 24 hours Experimental Results: At a concentration of 2 μM, both A549 and H1299 cells underwent G2/M phase arrest, while the number of cells in G1 or S phase decreased. At lower concentrations, H1299 cells underwent G1 phase arrest. Western Blot Analysis [1] Cell Types: A549, H1299 Non-small cell lung cancer (NSCLC) cells Tested Concentrations: 0.5 μM, 1 μM, 2 μM Incubation Duration: 24 hours Experimental Results: The protein levels of Cdc25C, p-Cdc25C, cyclin B1, and Cdc2 were significantly decreased in both cell lines. The protein level of γ-H2AX was significantly increased in both A549 and H1299 cells, indicating that DNA double-strand breaks were induced. In both A549 and H1299 cells, a dose-dependent increase in the cleavage of caspase-3, caspase-8, caspase-9, and PARP was observed. In both A549 and H1299 cells, dose-dependent decreases in the protein expression of p-Akt, total Akt, p-p70S6K, and total p70S6K were observed, indicating inhibition of the Akt/mTOR pathway. In both A549 and H1299 cells, dose-dependent decreases in the protein expression of YAP, TAZ, and survivin were observed, while dose-dependent increases in the protein expression of p-LATS1/2 were observed, indicating inhibition of the YAP/TAZ oncogenic axis.
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| Animal Protocol |
Animal/Disease Models:Female BALB/c nude mice (5 weeks old) were injected subcutaneously with CAOV3 cells (5×10⁶) on the ventral side [7]
Doses: 5 mg/kg Route of Administration: Intraperitoneal injection; once daily for 14 days Experimental Results: Tumor volume and weight were significantly reduced, and no physiologically harmful effects were caused to the mice. |
| References |
|
| Molecular Formula |
C21H18CLNO5
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|---|---|
| Molecular Weight |
399.82
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| Appearance |
Typically exists as solids at room temperature
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| SMILES |
CN1C2=C3C(C=C4OCOC4=C3)=CC=C2C5=C(C6=C(OCO6)C=C5)C1OC.Cl
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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|---|---|
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.5011 mL | 12.5056 mL | 25.0113 mL | |
| 5 mM | 0.5002 mL | 2.5011 mL | 5.0023 mL | |
| 10 mM | 0.2501 mL | 1.2506 mL | 2.5011 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.
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