JW 55

PARP domain inhibitor CAS# 664993-53-7

JW 55

Catalog No. BCC2453----Order now to get a substantial discount!

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Chemical structure

JW 55

3D structure

Chemical Properties of JW 55

Cas No. 664993-53-7 SDF Download SDF
PubChem ID 2946601 Appearance Powder
Formula C25H26N2O5 M.Wt 434.48
Type of Compound N/A Storage Desiccate at -20°C
Solubility DMSO : ≥ 50 mg/mL (115.08 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name N-[4-[[4-(4-methoxyphenyl)oxan-4-yl]methylcarbamoyl]phenyl]furan-2-carboxamide
SMILES COC1=CC=C(C=C1)C2(CCOCC2)CNC(=O)C3=CC=C(C=C3)NC(=O)C4=CC=CO4
Standard InChIKey ZJZWZIXSGNFWQQ-UHFFFAOYSA-N
Standard InChI InChI=1S/C25H26N2O5/c1-30-21-10-6-19(7-11-21)25(12-15-31-16-13-25)17-26-23(28)18-4-8-20(9-5-18)27-24(29)22-3-2-14-32-22/h2-11,14H,12-13,15-17H2,1H3,(H,26,28)(H,27,29)
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 JW 55

DescriptionInhibitor of the PARP domain of tankyrase 1 and 2 (TNKS1/2). Activity results in stabilization of Axin2 and increased degradation of β-catenin; inhibits the β-catenin signaling pathway. Also shown to decrease canonical Wnt signaling in SW480 and HCT-15 colon carcinoma cell lines; reduces cell cycle progression and proliferation in SW480 cells in vitro.

JW 55 Dilution Calculator

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JW 55 Molarity Calculator

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Preparing Stock Solutions of JW 55

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.3016 mL 11.508 mL 23.016 mL 46.032 mL 57.54 mL
5 mM 0.4603 mL 2.3016 mL 4.6032 mL 9.2064 mL 11.508 mL
10 mM 0.2302 mL 1.1508 mL 2.3016 mL 4.6032 mL 5.754 mL
50 mM 0.046 mL 0.2302 mL 0.4603 mL 0.9206 mL 1.1508 mL
100 mM 0.023 mL 0.1151 mL 0.2302 mL 0.4603 mL 0.5754 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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Background on JW 55

IC50: 1.9 μM (TNK S1); 0.83 μM (TNK S2)

Increased nuclear accumulation of β-catenin, a mediator of canonical Wnt signaling, is found in numerous tumors and is frequently associated with tumor progression and metastasis. Inhibition of Wnt/b-catenin signaling therefore is an attractive strategy for anticancer drugs.

In vitro: In a previous study, the authors identified a novel small molecule inhibitor of the β-catenin signaling pathway, JW55, that functions via inhibition of the PARP domain of tankyrase 1 and tankyrase 2 (TNKS1/2), regulators of the b-catenin destruction complex. Inhibition of TNKS1/2 poly(ADP-ribosyl)ation activity by JW55 led to stabilization of AXIN2, a member of the b-catenin destruction complex, followed by increased degradation of b-catenin. In a dose-dependent manner, JW55 inhibited canonical Wnt signaling in colon carcinoma cells that contained mutations in either the APC (adenomatous polyposis coli) locus or in an allele of b-catenin [1].

In vivo: JW55 was reported to reduce XWnt8-induced axis duplication in Xenopus embryos and tamoxifen-induced polyposis formation in conditional APC mutant mice. These findings provide a novel chemotype for targeting canonical Wnt/b-catenin signaling through inhibiting the PARP domain of TNKS1/2 [1].

Clinical trial: JW55 is currently in the preclinical development and no clinical trial is ongoing.

Reference:
[1] Waaler J, Machon O, Tumova L, Dinh H, Korinek V, Wilson SR, Paulsen JE, Pedersen NM, Eide TJ, Machonova O, Gradl D, Voronkov A, von Kries JP, Krauss S.  A novel tankyrase inhibitor decreases canonical Wnt signaling in colon carcinoma cells and reduces tumor growth in conditional APC mutant mice. Cancer Res. 2012;72(11):2822-32.

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References on JW 55

Performance on physical function tests and the risk of fractures and admissions: Findings from a national health screening of 557,648 community-dwelling older adults.[Pubmed:27810666]

Arch Gerontol Geriatr. 2017 Jan - Feb;68:174-180.

OBJECTIVE: Falls and fractures in older adults are often preventable, yet remain major health concerns as comprehensive physical function assessment may not be readily available. This study investigated whether simple timed up and go test (TUG) and unipedal stance test (UST) are effective in identifying people with an increased risk of fractures, femoral fractures, or admissions due to femoral fractures. METHODS: Community-dwelling Korean older adults aged 66 years participated in the Korean National Screening Program for the Transitional Ages (n=557,648) between 2007 and 2010. Overall fractures, femoral fractures, and admissions due to femoral fracture during this period were outcome measures. The outcome measures were overall fractures, femoral fractures, and admissions due to femoral fracture after the health screening. The associations between inferior physical function test results and outcome measures were evaluated. RESULTS: A total of 523,502 subjects were followed-up for a mean period of 1.42 years, which resulted in 12,965 subjects with any fractures. Fracture data were retrieved from medical claims record. Subjects who performed poorly on one or both of the two physical function tests experienced higher number of overall fractures (aHR 1.21, 95% CI: 1.16-1.26), femoral fractures (aHR 1.80, 95% CI: 1.59-2.17), and admissions due to femoral fractures (aHR 1.85, 95% CI: 1.55-2.22) as compared to subjects with normal results on both tests. Combining TUG and UST was not superior to performing UST alone in predicting the increased risk of overall fractures (p=0.347), femoral fractures (p=0.402) or admissions due to femoral fractures (p=0.774). CONCLUSIONS: Poor performance on physical performance tests is associated with a higher risk of overall fractures, femoral fractures and admissions due to femoral fractures. The TUG and UST can be used to identify community-dwelling older individuals who are more vulnerable to fractures.

Vitamin D levels and deficiency with different occupations: a systematic review.[Pubmed:28637448]

BMC Public Health. 2017 Jun 22;17(1):519.

BACKGROUND: Vitamin D deficiency is prevalent worldwide, but some groups are at greater risk. We aim to evaluate vitamin D levels in different occupations and identify groups vulnerable to vitamin D deficiency. METHODS: An electronic search conducted in Medline, Embase, the Cochrane Central Register of Controlled Trials, and CINAHL Plus with Full Text generated 2505 hits; 71 peer-reviewed articles fulfilled the inclusion criteria. Occupations investigated included outdoor and indoor workers, shiftworkers, lead/smelter workers, coalminers, and healthcare professionals. We calculated the pooled average metabolite level as mean +/- SD; deficiency/insufficiency status was described as % of the total number of subjects in a given category. RESULTS: Compared to outdoor workers, indoor workers had lower 25-hydroxyvitamin D (25-(OH)D) levels (40.6 +/- 13.3 vs. 66.7 +/- 16.7 nmol/L; p < 0.0001). Mean 25-(OH)D levels (in nmol/L) in shiftworkers, lead/smelter workers and coalminers were 33.8 +/- 10.0, 77.8 +/- 5.4 and 56.6 +/- 28.4, respectively. Vitamin D deficiency (25-(OH)D < 50 nmol/L), was high in shiftworkers (80%) and indoor workers (78%) compared to outdoor workers (48%). Among healthcare professionals, medical residents and healthcare students had the lowest levels of mean 25-(OH)D, 44.0 +/- 8.3 nmol/L and 45.2 +/- 5.5 nmol/L, respectively. The mean 25-(OH)D level of practising physicians, 55.0 +/- 5.8 nmol/L, was significantly different from both medical residents (p < 0.0001) and healthcare students (p < 0.0001). Nurses and other healthcare employees had 25-(OH)D levels of 63.4 +/- 4.2 nmol/L and 63.0 +/- 11.0 nmol/L, respectively, which differed significantly compared to practising physicians (p = 0.01), medical residents (p < 0.0001) and healthcare students (p < 0.0001). Rates of vitamin D deficiency among healthcare professionals were: healthcare students 72%, medical residents 65%, practising physicians 46%, other healthcare employees 44%, and nurses 43%. Combined rates of vitamin D deficiency or insufficiency (25-(OH)D < 75 nmol/L) were very high in all investigated groups. Potential confounders such as gender and body composition were not consistently reported in the primary studies and were therefore not analyzed. Furthermore, the descriptions of occupational characteristics may be incomplete. These are limitations of our systematic review. CONCLUSIONS: Our review demonstrates that shiftworkers, healthcare workers and indoor workers are at high risk to develop vitamin D deficiency, which may reflect key lifestyle differences (e.g. sunlight exposure). This may help target health promotion and preventive efforts.

Lipoprotein-associated phospholipase A2 in coronary heart disease: Review and meta-analysis.[Pubmed:27956130]

Clin Chim Acta. 2017 Feb;465:22-29.

BACKGROUND: Risk associations between lipoprotein-associated phospholipase A2 (Lp-PLA2) and adverse outcomes in patients with coronary heart disease (CHD) remain unclear. The aim of the meta-analysis was to investigate the association between Lp-PLA2 and prognosis of CHD. METHODS: PubMed and Embase were examined for prospective studies published before June 2016. Multivariate-adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) for the risk of adverse outcomes according to Lp-PLA2 activity or mass were extracted, pooled, and weighted using generic inverse-variance and random-effect modeling. RESULTS: Fifteen studies with 30,857 participants were included. Overall, higher Lp-PLA2 activity or mass was not significantly related to increased risk of long-term all-cause mortality. However, higher Lp-PLA2 activity or mass was independently associated with an increased risk of long-term cardiovascular events, with pooled HR for cardiovascular events of 1.55 (95% CI, 1.08-2.23; P=0.018) and 1.62 (95% CI, 1.09-2.41; P=0.017), respectively. The prognostic value of Lp-PLA2 in predicting cardiovascular events was observed in patients with stable CHD who were not receiving therapies for inhibiting Lp-PLA2. CONCLUSIONS: Greater Lp-PLA2 activity or mass was independently associated with cardiovascular events in patients with CHD, particularly in patients with stable CHD who were not receiving therapies for inhibiting Lp-PLA2.

Insulin-like growth factor 1 receptor activation promotes mammary gland tumor development by increasing glycolysis and promoting biomass production.[Pubmed:28173837]

Breast Cancer Res. 2017 Feb 7;19(1):14.

BACKGROUND: The insulin-like growth factor 1 (IGF1) signaling axis plays a major role in tumorigenesis. In a previous experiment, we chronically treated mice with several agonists of the IGF1 receptor (IGF1R). We found that chronic treatment with insulin analogues with high affinity towards the IGF1R (IGF1 and X10) decreased the mammary gland tumor latency time in a p53(R270H/+)WAPCre mouse model. Frequent injections with insulin analogues that only mildly activated the IGF1R in vivo (glargine and insulin) did not significantly decrease the tumor latency time in this mouse model. METHODS: Here, we performed next-generation RNA sequencing (40 million, 100 bp reads) on 50 mammary gland tumors to unravel the underlying mechanisms of IGF1R-promoted tumorigenesis. Mutational profiling of the individual tumors was performed to screen for treatment-specific mutations. The transcriptomic data were used to construct a support vector machine (SVM) classifier so that the phenotypic characteristics of tumors exposed to the different insulin analogue treatments could be predicted. For translational purposes, we ran the same classifiers on transcriptomic (micro-array) data of insulin analogue-exposed human breast cancer cell lines. Genome-scale metabolic modeling was performed with iMAT. RESULTS: We found that chronic X10 and IGF1 treatment resulted in tumors with an increased and sustained proliferative and invasive transcriptomic profile. Furthermore, a Warburg-like effect with increased glycolysis was observed in tumors of the X10/IGF1 groups and, to a lesser extent, also in glargine-induced tumors. A metabolic flux analysis revealed that this enhanced glycolysis programming in X10/IGF1 tumors was associated with increased biomass production programs. Although none of the treatments induced genetic instability or enhanced mutagenesis, mutations in Ezh2 and Hras were enriched in X10/IGF1 treatment tumors. CONCLUSIONS: Overall, these data suggest that the decreased mammary gland tumor latency time caused by chronic IGF1R activation is related to modulation of tumor progression rather than increased tumor initiation.

Validated high-performance liquid chromatography method for the determination of the inhibitor of cancer cell invasion (E)-N-benzyl-6-[2-(3, 4-dihydroxy benzylidene)hydrazinyl]-N-methylpyridine-3-sulfonamide in rat plasma and its application to pharmacokinetic study.[Pubmed:27809343]

Biomed Chromatogr. 2017 May;31(5).

In this study, a reliable method for the quantitation of (E)-N-benzyl-6-[2-(3, 4-dihydroxy benzylidene)hydrazinyl]-N-methylpyridine-3-sulfonamide (JW-55) in rat plasma was developed and validated using high-performance liquid chromatography. Plasma samples were deproteinized; sildenafil was used as an internal standard. Chromatographic separation was achieved using a reversed-phase C18 column. The mobile phase, 0.02 m ammonium acetate buffer:acetonitrile (48:52, v/v), was run at a flow rate of 1.0 mL/min at room temperature, and the column eluent was monitored using an ultraviolet detector at 280 nm. The retention times of JW-55 and sildenafil were ~5.9 and 7.7 min, respectively. The detection limit of JW-55 in rat plasma was 0.03 mug/mL. Pharmacokinetic parameters of JW-55 were evaluated after intravenous and oral administration of JW-55 (10 mg/kg) in rats. After oral administration, the F value was approximately 73.7%.

A novel tankyrase inhibitor decreases canonical Wnt signaling in colon carcinoma cells and reduces tumor growth in conditional APC mutant mice.[Pubmed:22440753]

Cancer Res. 2012 Jun 1;72(11):2822-32.

Increased nuclear accumulation of beta-catenin, a mediator of canonical Wnt signaling, is found in numerous tumors and is frequently associated with tumor progression and metastasis. Inhibition of Wnt/beta-catenin signaling therefore is an attractive strategy for anticancer drugs. In this study, we have identified a novel small molecule inhibitor of the beta-catenin signaling pathway, JW55, that functions via inhibition of the PARP domain of tankyrase 1 and tankyrase 2 (TNKS1/2), regulators of the beta-catenin destruction complex. Inhibition of TNKS1/2 poly(ADP-ribosyl)ation activity by JW55 led to stabilization of AXIN2, a member of the beta-catenin destruction complex, followed by increased degradation of beta-catenin. In a dose-dependent manner, JW55 inhibited canonical Wnt signaling in colon carcinoma cells that contained mutations in either the APC (adenomatous polyposis coli) locus or in an allele of beta-catenin. In addition, JW55 reduced XWnt8-induced axis duplication in Xenopus embryos and tamoxifen-induced polyposis formation in conditional APC mutant mice. Together, our findings provide a novel chemotype for targeting canonical Wnt/beta-catenin signaling through inhibiting the PARP domain of TNKS1/2.

Description

JW 55 is a potent and selective β-catenin signaling pathway inhibitor, which functions via inhibition of the PARP domain of tankyrase 1 and tankyrase 2 (TNKS1/2). JW 55 decreases auto-PARsylation of TNKS1/2 in vitro with IC50s of 1.9 μM and 830 nM respectively.

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