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iMDK

Suppressor of MDK expression; inhibits PI 3-K signaling CAS# 881970-80-5

iMDK

Catalog No. BCC6365----Order now to get a substantial discount!

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iMDK: 5mg $115 In Stock
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Chemical structure

iMDK

3D structure

Chemical Properties of iMDK

Cas No. 881970-80-5 SDF Download SDF
PubChem ID 15991416 Appearance Powder
Formula C21H13FN2O2S M.Wt 376.4
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 5 mM in DMSO
Chemical Name 3-[2-[(4-fluorophenyl)methyl]imidazo[2,1-b][1,3]thiazol-6-yl]chromen-2-one
SMILES C1=CC=C2C(=C1)C=C(C(=O)O2)C3=CN4C=C(SC4=N3)CC5=CC=C(C=C5)F
Standard InChIKey IWFKQTWYILKFGE-UHFFFAOYSA-N
Standard InChI InChI=1S/C21H13FN2O2S/c22-15-7-5-13(6-8-15)9-16-11-24-12-18(23-21(24)27-16)17-10-14-3-1-2-4-19(14)26-20(17)25/h1-8,10-12H,9H2
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of iMDK

DescriptionSuppressor of endogenous midkine (MDK) expression. Inhibits PI 3-K signaling in H441 lung adenocarcinoma cells. Selectively attenuates growth of MDK-expressing cancer cells. Induces apoptosis in H441 cells and suppresses growth of H441 cell xenografts in mice.

iMDK Dilution Calculator

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iMDK Molarity Calculator

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Preparing Stock Solutions of iMDK

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.6567 mL 13.2837 mL 26.5675 mL 53.135 mL 66.4187 mL
5 mM 0.5313 mL 2.6567 mL 5.3135 mL 10.627 mL 13.2837 mL
10 mM 0.2657 mL 1.3284 mL 2.6567 mL 5.3135 mL 6.6419 mL
50 mM 0.0531 mL 0.2657 mL 0.5313 mL 1.0627 mL 1.3284 mL
100 mM 0.0266 mL 0.1328 mL 0.2657 mL 0.5313 mL 0.6642 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on iMDK

Novel Midkine Inhibitor iMDK Inhibits Tumor Growth and Angiogenesis in Oral Squamous Cell Carcinoma.[Pubmed:27272788]

Anticancer Res. 2016 Jun;36(6):2775-81.

Midkine is a heparin-binding growth factor highly expressed in various human malignant tumors. However, its role in the growth of oral squamous cell carcinoma is not well understood. In this study, we analyzed the antitumor effect of a novel midkine inhibitor (iMDK) against oral squamous cell carcinoma. Administration of iMDK induced a robust antitumor response and suppressed cluster of differentiation 31 (CD31) expression in oral squamous cell carcinoma HSC-2 cells and SAS cells xenograft models. iMDK inhibited the proliferation of these cells dose-dependently, as well as the expression of midkine and phospho-extracellular signal-regulated kinase in HSC-2 and SAS cells. Moreover, iMDK significantly inhibited vascular endothelial growth factor and induced tube growth of human umbilical vein endothelial cells in a dose-dependent fashion. These findings suggest that midkine is critically involved in oral squamous cell carcinoma and iMDK can be effectively used for the treatment of oral squamous cell carcinoma.

A novel PI3K inhibitor iMDK suppresses non-small cell lung Cancer cooperatively with A MEK inhibitor.[Pubmed:25839409]

Exp Cell Res. 2015 Jul 15;335(2):197-206.

The PI3K-AKT pathway is expected to be a therapeutic target for non-small cell lung cancer (NSCLC) treatment. We previously reported that a novel PI3K inhibitor iMDK suppressed NSCLC cells in vitro and in vivo without harming normal cells and mice. Unexpectedly, iMDK activated the MAPK pathway, including ERK, in the NSCLC cells. Since iMDK did not eradicate such NSCLC cells completely, it is possible that the activated MAPK pathway confers resistance to the NSCLC cells against cell death induced by iMDK. In the present study, we assessed whether suppressing of iMDK-mediated activation of the MAPK pathway would enhance anti-tumorigenic activity of iMDK. PD0325901, a MAPK inhibitor, suppressed the MAPK pathway induced by iMDK and cooperatively inhibited cell viability and colony formation of NSCLC cells by inducing apoptosis in vitro. HUVEC tube formation, representing angiogenic processes in vitro, was also cooperatively inhibited by the combinatorial treatment of iMDK and PD0325901. The combinatorial treatment of iMDK with PD0325901 cooperatively suppressed tumor growth and tumor-associated angiogenesis in a lung cancer xenograft model in vivo. Here, we demonstrate a novel treatment strategy using iMDK and PD0325901 to eradicate NSCLC.

Inhibition of the growth factor MDK/midkine by a novel small molecule compound to treat non-small cell lung cancer.[Pubmed:23976985]

PLoS One. 2013 Aug 16;8(8):e71093.

Midkine (MDK) is a heparin-binding growth factor that is highly expressed in many malignant tumors, including lung cancers. MDK activates the PI3K pathway and induces anti-apoptotic activity, in turn enhancing the survival of tumors. Therefore, the inhibition of MDK is considered a potential strategy for cancer therapy. In the present study, we demonstrate a novel small molecule compound (iMDK) that targets MDK. iMDK inhibited the cell growth of MDK-positive H441 lung adenocarcinoma cells that harbor an oncogenic KRAS mutation and H520 squamous cell lung cancer cells, both of which are types of untreatable lung cancer. However, iMDK did not reduce the cell viability of MDK-negative A549 lung adenocarcinoma cells or normal human lung fibroblast (NHLF) cells indicating its specificity. iMDK suppressed the endogenous expression of MDK but not that of other growth factors such as PTN or VEGF. iMDK suppressed the growth of H441 cells by inhibiting the PI3K pathway and inducing apoptosis. Systemic administration of iMDK significantly inhibited tumor growth in a xenograft mouse model in vivo. Inhibition of MDK with iMDK provides a potential therapeutic approach for the treatment of lung cancers that are driven by MDK.

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