| Field | Specification |
|---|---|
| Alternative names | endo-IWR 1; IWR-1-endo |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C25H19N3O3 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
IWR-1, also known as IWR-1-endo or endo-IWR 1, is a tankyrase inhibitor that targets Wnt/β-catenin signaling with an IC50 of 180 nM. It disrupts key steps of canonical Wnt signaling, including translocation of β-catenin to the nucleus and the subsequent TCF/LEF activation and expression of Wnt/β-catenin downstream targets, and it promotes β-catenin phosphorylation by stabilizing Axin-scaffolded destruction complexes. It can be studied for antitumor purposes and in diseases such as osteosarcoma, colorectal cancer, and psoriasis[1][2][4]. It is supplied as an off-white to yellow solid (C25H19N3O3, MW 409.44) at 99.60% purity.
Physical & Chemical Properties
| CAS Number | 1127442-82-3 |
|---|---|
| Molecular Formula | C25H19N3O3 |
| Molecular Weight | 409.44 g/mol |
| Purity | 99.60% |
| Appearance | Solid |
| Color | Off-white to yellow |
| SMILES | O=C(NC1=C2N=CC=CC2=CC=C1)C3=CC=C(N(C([C@]4([H])[C@](C5)([H])C=C[C@]5([H])[C@]64[H])=O)C6=O)C=C3 |
| Signaling Pathway | Stem Cell/Wnt |
| Solubility | In Vitro: DMSO: 50 mg/mL (122.12 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 2 years; -20°C, 1 year. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target
IC50: 180 nM (Wnt)
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
[2]. Lee SC, et al., IWR-1 inhibits epithelial-mesenchymal transition of colorectal cancer cells through suppressing Wnt/β-catenin signaling as well as survivin expression. Oncotarget. 2015 Sep 29;6(29):27146-59.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 50 mg/mL (122.12 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 2 years) or -20°C (up to 1 year); avoid repeated freeze-thaw cycles.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 2.5 mg/mL (6.11 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Protocol 2
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | ≥ 2.5 mg/mL (6.11 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 3
| Composition | 10% DMSO + 90% Corn Oil |
|---|---|
| Result | ≥ 2.5 mg/mL (6.11 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL corn oil. |
Data provided by the manufacturer.
In Vitro
IWR-1 exerts cytotoxicity on osteosarcoma cancer stem-like cells (CSCs)[1]. In colorectal cancer cell lines, cell migration, invasion, and matrix metalloproteinase activities are suppressed by IWR-1[2]. In parental cells and in spheres from MG-63 and MNNG-HOS cell lines, IWR-1 (2.5-10 μM, 48-96 h) effectively reduces the viability of spheres, in a concentration- and time- dependent manner[1]. TUNEL-positive cell numbers rise with IWR-1 (10 μM, 96 h), reaching 4.65- and 15.83-fold differences relative to control at 96 h, and activation of caspases 3/7 is promoted, reaching 2.15- and 1.27-fold in MG-63 and MNNG-HOS spheres[1]. In spheres derived from MG-63 and MNNG-HOS cell lines, IWR-1 (10 μM, 48 h) induces cell cycle arrest in the G2/M phase and slightly increases the percentage of cells in the S phase[1]. In MG-6t4 and MNNG-HOS cells, secondary sphere-forming efficacy is inhibited by IWR-1 (10 μM, 48 h) by approximately 53% and 55% of the first-generation 7-day old spheres[1]. Proliferation of HCT116 cells is decreased by IWR-1 (5-50 μM, 24-48 h) in a dose- and time-dependent manner[2]. TNF-α-stimulated migration in HCT116 and HT29 cells is inhibited by IWR-1 (5-50 μM, 24-48 h)[2].
Western Blot Analysis[1]
| Cell Line | MG-63 and MNNG-HOS spheres and parent cells |
|---|---|
| Concentration | 10 μM |
| Incubation Time | 96 h |
| Result | Led to an upregulation of Bak and a downregulation of Bcl-2 (key proteins involved in mitochondrial-dependent apoptosis), which contributes to a Bak/Bcl-2 ratio >1 that prone the cells to undergo apoptosis. Resulted in a higher β-catenin nuclear/cytoplasmic ratio in spheres, indicating an increased Wnt/β-catenin pathway activation in osteosarcoma spheres. Stabilized Axin2 protein levels. Diminished the protein expression levels of Cyclin D1 in both parental cells and spheres. |
RT-PCR[1]
| Cell Line | MG-63 and MNNG-HOS spheres and parent cells |
|---|---|
| Concentration | 10 μM |
| Incubation Time | 96 h |
| Result | Led to an upregulation of Bak and a downregulation of Bcl-2 (key proteins involved in mitochondrial-dependent apoptosis), which contributes to a Bak/Bcl-2 ratio >1 that prone the cells to undergo apoptosis. Results in a higher β-catenin nuclear/cytoplasmic ratio in spheres, indicating an increased Wnt/β-catenin pathway activation in osteosarcoma spheres. Stabilized Axin2 protein levels. Diminished the protein expression levels of Cyclin D1 in both parental cells and spheres. |
Cell Viability Assay[1]
| Cell Line | MG-63 and MNNG-HOS spheres and parent cells |
|---|---|
| Concentration | 2.5, 5, 7.5, 10 μM |
| Incubation Time | 48 and 96 h |
| Result | Reduced cell viability when concentration is higher than 5 μM. Elicited more than 70% reduction of cell viability in spheres derived from the two cell lines at 96 h with 10 μM. Had minimal effect on parental cells since the Wnt/β-catenin signaling is absent in these cells. Increased the susceptibility of spheres towards Doxorubicin when treated in combination with increasing concentrations of Doxorubicin (0.01-100 μM). |
Western Blot Analysis[2]
| Cell Line | HCT116 cells |
|---|---|
| Concentration | 5, 10, 20, 50 μM |
| Incubation Time | 0, 4, 8, 24, 48 h |
| Result | Increased the levels of the epithelial marker E-cadherin whilst decreased the mesenchymal markers N-cadherin, Vimentin, and Snail dose- and time-dependently. Inhibited the EMT process in HCT116 cells effectively. Decreased β-catenin expression and inhibited the EMT-like expressional changes whereby decreasing N-cadherin and Snail and increasing E-cadherin expressions, even in the presence of TNF-α (10 ng/mL for 24 h)-induced EMT stimulation. Decreased the phosphorylation of Akt in a concentration- and time-dependent manner. Decreased the surviving expression in a concentration- and time-dependent manner, thereby promoting tumor proliferation directly or indirectly through regulating cancer cell homeostasis. Reduced MMP activities only when surviving was suppressed. |
Real Time qPCR[2]
| Cell Line | HCT116 cells |
|---|---|
| Concentration | 5, 10, 20, 50 μM |
| Incubation Time | 0, 4, 8, 24, 48 h |
| Result | Inhibited EMT in the mRNA levels under the TNF-α-induced EMT stimulation. |
In Vivo
In an osteosarcoma mouse model, IWR-1 (5 mg/kg, intratumorally, each 2 d for 12 d) induces marked inhibition of tumor growth[1]. In an Imiquimod (IMQ)-induced psoriasis-like mouse model, IWR-1 (10 mg/kg, s.c., on days 1, 3, 5) ameliorates exacerbation of psoriatic skin lesions mediated by IL-36γ (2 μg/mouse on days 1, 3, 5)[3].
| Animal Model | Immunocompromised nude mice (6-week old female Swiss nude) were injected sub-cutaneously the pGL4-transfected MNNG-HOS cells (2×106 cells/100 mL PBS)[1] |
|---|---|
| Dosage | 5 mg/kg |
| Administration | Intratumorally, each 2 d for 12 d |
| Result | Resulted in slower tumor growth rate and reduction in tumor size by 73% and 71% in comparison to control and to Doxorubicin-treated (8 mg/kg, i.p., each 4 d for 12 d) groups. Enhanced the therapeutic efficacy of Doxorubicin shown by a greater reduction of tumor burden at the end of the treatment in opposite to Doxorubicin alone. |
| Animal Model | Balb/c mice (aged 6-8 weeks) with shaven back and treated with a daily topical dose of IMQ cream[3] |
|---|---|
| Dosage | 10 mg/kg |
| Administration | Subcutaneous injection (s.c.) on days 1, 3, 5 |
| Result | Increased epidermal thickening with keratinocyte thickness. Significantly diminished the effect of IMQ on hyperplasia in the IMQ+IWR-1 group. Ameliorated the pathological changes in IL-36γ-induced psoriasiform skin lesion. Reversed IL-36γ-mediated upregulation of inflammatory factors (IL-17 A and IFN-γ) in psoriatic lesions. Reversed IL-36γ-mediated upregulation of β-catenin and DKK1 expression. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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