Physicochemical Properties
| Molecular Formula | C24H23NO3S |
| Molecular Weight | 405.509325265884 |
| Exact Mass | 405.139 |
| CAS # | 2447607-85-2 |
| PubChem CID | 169450734 |
| Appearance | White to off-white solid powder |
| LogP | 5.9 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 3 |
| Rotatable Bond Count | 4 |
| Heavy Atom Count | 29 |
| Complexity | 640 |
| Defined Atom Stereocenter Count | 0 |
| InChi Key | FBLPWEPWFONTID-UHFFFAOYSA-N |
| InChi Code | InChI=1S/C24H23NO3S/c1-16-8-10-21(11-9-16)29(27,28)25-15-20(22-6-4-5-7-23(22)25)14-19-12-17(2)24(26)18(3)13-19/h4-13,15,26H,14H2,1-3H3 |
| Chemical Name | 2,6-dimethyl-4-[[1-(4-methylphenyl)sulfonylindol-3-yl]methyl]phenol |
| 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 |
| Shipping Condition | Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs) |
Biological Activity
| ln Vitro | In GL216 cells, ALK-IN-26 (0.5-2 μM, 24 h) can suppress ALK activity [1]. In GL216, U87MG, and Hela cells, ALK-IN-26 (0.5–10 μM, 24-72 h) can suppress GL216 and U87MG activity, but it has little effect on Hela cell activity [1]. In GL216 cells, mTOR protein expression can be decreased by ALK-IN-26 (0.5-2 μM, 24 h) [1]. In both GL261 and U87MG cells, ALK-IN-26 (0.5-2 μM, 24 h) markedly decreased the levels of p-ERK1/2 protein, increased those of p-JNK, and had no effect on p-AKT or p-STAT3 protein[1]. In GL261 cells, autophagy can be induced by ALK-IN-26 (0.5-2 μM, 24 h) [1]. In GL261 cells, cleaved-PARP (c-PARP) and cleaved-caspase-3 (c-caspase 3) protein levels are elevated by ALK-IN-26 (0.5 μM-2 μM, 24-72 h) [1]. GL261 cells undergo apoptosis in response to ALK-IN-26 (0.5 μM–2 μM, 24-72 h) [1]. |
| ln Vivo | Male C57BL6/J mice exhibit the pharmacokinetic characteristics of ALK-IN-26 (5 mg/kg, iv, single dose)[1]. In male C57BL6/J mice, ALK-IN-26 (20 mg/kg, ip, single dose) can cross the blood-brain barrier[1]. Male C57BL6/J mice were used for the pharmacokinetic analysis[1]; the pharmacokinetic properties were T1/2(h) Tmax(h) Cmax (ng/mL) AUC(0-8) (h*ng/mL) AUC(0 -∞) (h*ng/mL) MRT(0-8) (h) MRT(0-∞) (h) V∞ (L/kg) V2 (L/kg) bioavailability F (%) iv(5mg/kg) 1.13 0.08 1978.21 884.88 924.56 0.63 0.84 4.59 8.40 ip(5mg/kg) 3.55 0.58 117.57 339.79 420.50 2.25 4.60 / / / / |
| Cell Assay |
Apoptosis Analysis[1] Cell Types: GL261 Tested Concentrations: 0.5 μM, 1.0 μM, 2.0 μM Incubation Duration: 24 h, 48 h, 72 h Experimental Results: Induced apoptosis of glioblastoma in a concentration- and time-dependent manner, and caused the cells (24.5%) entered the S phase but barely proceeded to the G2/M phase when treated with 1 μM for 72 h. Cell Viability Assay[1] Cell Types: GL216, U87MG, Hela Tested Concentrations: 0.5 μM, 1.0 μM, 2.0 μM , 5 μM, 10 μM for GL216 and U87MG cells 5 μM, 10 μM, 20 μM, 40 μM, 80 μM, 160 μM for Hela cells Incubation Duration: 24 h, 48h, 72h Experimental Results: Inhibited the activity of GL216 cells with the inhibition rate of cells at 80% when incubated with 2 μM for 72 h and inhibited U87MG cells viability with a dose- and time-dependent manner, while demonstrated limited inhibition on Hela cells, even at 160 μM, the inhibition rate is less than 50 %. Can inhibit the activity of ALK tyrosine kinase with a dose-dependent manner. Cell Autophagy Assay[1] Cell Types: GL261 Tested Concentrations: 0.5 μM, 1.0 μM, 2.0 μM Inc |
| Animal Protocol |
Animal/Disease Models: Male C57BL/6 J mice[1] Doses: 5 mg/kg Route of Administration: intravenous (iv) injection ( iv), Single dose Experimental Results: Could be rapidly absorbed (Tmax = 0.58 h) with an acceptable half-life (T1/2 = 3.55 h) and bioavailability (F = 38.4%). Animal/Disease Models: Male C57BL/6J mice[1] Doses: 20mg/kg Route of Administration: intraperitoneal (ip) injection (ip), Single dose Experimental Results: Could enter the body at concentrations up to 2.7μmol/kg (after 2 h administration at 20 mg/kg) and penetrate the blood-brain barrier. |
| References |
[1]. Synthesis and Bioevaluation of 3-(Arylmethylene) indole Derivatives: Discovery of a Novel ALK Modulator with Antiglioblastoma Activities. Journal of Medicinal Chemistry, 2023. |
Solubility Data
| 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 |
| 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 (e.g. IP/IV/IM/SC) Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline) *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). 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)] *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. Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline) Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline) Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline) Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil) Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL 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). Oral Formulation 3: Dissolved in PEG400 Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose Oral Formulation 6: Mixing with food powders Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.4660 mL | 12.3302 mL | 24.6603 mL | |
| 5 mM | 0.4932 mL | 2.4660 mL | 4.9321 mL | |
| 10 mM | 0.2466 mL | 1.2330 mL | 2.4660 mL |