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Foxy-5 Sale

(Synonyms: N-甲酰-L-甲酰-L-Α-天冬氨酸-甘氨酸-L-胱氨酸-L-Α-谷氨酰胺-L-亮氨酸) 目录号 : GC36073

A Wnt5a peptide mimetic

Foxy-5 Chemical Structure

Cas No.:881188-51-8

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产品描述

Foxy-5 is a Wnt5a peptide mimetic with anticancer activity.1,2 It increases adhesion and reduces cell motility of MDA-MB-468 breast cancer cells when used at concentrations ranging from 1 to 1,000 ?M.1 Foxy-5 (2 mg/kg) reduces the number of lymph node metastases without affecting primary tumor growth in a DU145-Luc mouse xenograft model.2

1.S?fholm, A., Leandersson, K., Dejmek, J., et al.A formylated hexapeptide ligand mimics the ability of Wnt-5a to impair migration of human breast epithelial cellsJ. Biol. Chem.281(5)2740-2749(2006) 2.Canesin, G., Evans-Axelsson, S., Hellsten, R., et al.Treatment with the WNT5A-mimicking peptide Foxy-5 effectively reduces the metastatic spread of WNT5A-low prostate cancer cells in an orthotopic mouse modelPLoS One12(9)e0184418(2017)

Chemical Properties

Cas No. 881188-51-8 SDF
别名 N-甲酰-L-甲酰-L-Α-天冬氨酸-甘氨酸-L-胱氨酸-L-Α-谷氨酰胺-L-亮氨酸
分子式 C26H42N6O12S2 分子量 694.77
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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1 mM 1.4393 mL 7.1966 mL 14.3933 mL
5 mM 0.2879 mL 1.4393 mL 2.8787 mL
10 mM 0.1439 mL 0.7197 mL 1.4393 mL
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Research Update

The WNT-5a derived peptide, Foxy-5, possesses dual properties that impair progression of ERalpha negative breast cancer

Cell Cycle 2009 Jun 15;8(12):1838-42.PMID:19448401DOI:10.4161/cc.8863.

Despite improvements in detection and treatment, breast cancer remains the most common female cancer worldwide, and metastatic associated mortality is a significant public health issue. Patients with tumors negative for estrogen receptor (ERalpha), have a particularly poor prognosis, partly due to their inability to respond to current endocrine treaments. Expression of Wnt-5a has been associated with prolonged recurrence free survivial in clinical material, and Wnt-5a also inhibits migration and invasion of breast cancer cell lines. Loss of Wnt-5a is associated with loss of ERalpha in clinical breast cancer material, and Wnt-5a signaling upregulates ERalpha in ERalpha negative breast cancer cell lines. A Wnt-5a derived hexapeptide, Foxy-5, has been developed and like Wnt-5a, increases adhesion and inhibits migration of breast cancer cells. Furthermore, Foxy-5 significantly reduced liver and lung metastases in a murine ERalpha negative breast cancer model. Foxy-5 also upregulated ERalpha in this in vivo model and most significantly, in vitro rendered cells responsive to the selective estrogen receptor modulator, Tamoxifen. Together these studies suggest that Foxy-5 may be a potential new supplementary treatment for ERalpha negative breast cancer patients, as it addresses two of the most important aspects of cancer related mortality -- non response to endocrine therapy and metastasis.

Retracted manuscript: The WNT-5a derived peptide, Foxy-5, possesses dual properties that impair progression of ERα negative breast cancer

Cell Cycle 2011 Apr 1;10(7):1167.PMID:21430443DOI:10.4161/cc.10.7.15488.

Retraction for: "The WNT-5a derived peptide, Foxy-5, possesses dual properties that impair progression of ERa negative breast cancer," by Caroline E. Ford, Elin J. Ekström, Jillian Howlin and Tommy Andersson, which appeared in the June 15, 2009 issue of Cell Cycle (Ford CE, et al. Cell Cycle 2009; 8:1838-1842; 10.4161/cc.8.12.8863). The authors wish to note the following: "Recently a paper, on which I was the senior author and that was published in the Proceedings of the National Academy of Sciences titled "Wnt-5a signaling restores tamoxifen sensitivity in estrogen receptor-negative breast cancer cells" (Ford CE, Ekström EJ, Andersson T. Proc Natl Acad Sci USA 2009; 106:3919-24) was retracted. The fact that this paper was the direct reason for our review article in the Cell Cycle journal makes it logical that I also retract the cited review article published in the Cell Cycle journal, the other authors approve this retraction. We apologize for any inconvenience this may have caused."

The Wnt-5a-derived hexapeptide Foxy-5 inhibits breast cancer metastasis in vivo by targeting cell motility

Clin Cancer Res 2008 Oct 15;14(20):6556-63.PMID:18927296DOI:10.1158/1078-0432.CCR-08-0711.

Purpose: An inherent problem in breast cancer treatment is that current therapeutic approaches fail to specifically target the dissemination of breast cancer cells from the primary tumor. Clinical findings show that the loss of Wnt-5a protein expression in the primary breast tumor predicts a faster tumor spread, and in vitro analyses reveal that it does so by inhibiting tumor cell migration. Therefore, we hypothesized that the reconstitution of Wnt-5a signaling could be a novel therapeutic strategy to inhibit breast cancer metastasis. Experimental design: We used in vitro techniques to show that 4T1 mouse breast cancer cells responded to the reconstitution of Wnt-5a signaling using our novel Wnt-5a mimicking hexapeptide, Foxy-5, in the same way as human breast cancer cells. Therefore, we could subsequently study its effect in vivo on the metastatic spread of cancer following the inoculation of 4T1 cells into mice. Results: In vitro analyses revealed that both recombinant Wnt-5a and the Wnt-5a-derived Foxy-5 peptide impaired migration and invasion without affecting apoptosis or proliferation of 4T1 breast cancer cells. The in vivo experiments show that i.p. injections of Foxy-5 inhibited metastasis of inoculated 4T1 breast cancer cells from the mammary fat pad to the lungs and liver by 70% to 90%. Conclusions: These data provide proof of principle that the reconstitution of Wnt-5a signaling in breast cancer cells is a novel approach to impair breast tumor metastasis by targeting cell motility. In combination with existing therapies, this approach represents a potential novel therapeutic strategy for the treatment of breast cancer patients.

Treatment with the WNT5A-mimicking peptide Foxy-5 effectively reduces the metastatic spread of WNT5A-low prostate cancer cells in an orthotopic mouse model

PLoS One 2017 Sep 8;12(9):e0184418.PMID:28886116DOI:10.1371/journal.pone.0184418.

Prostate cancer patients with high WNT5A expression in their tumors have been shown to have more favorable prognosis than those with low WNT5A expression. This suggests that reconstitution of Wnt5a in low WNT5A-expressing tumors might be an attractive therapeutic approach. To explore this idea, we have in the present study used Foxy-5, a WNT5A mimicking peptide, to investigate its impact on primary tumor and metastasis in vivo and on prostate cancer cell viability, apoptosis and invasion in vitro. We used an in vivo orthotopic xenograft mouse model with metastatic luciferase-labeled WNT5A-low DU145 cells and metastatic luciferase-labeled WNT5A-high PC3prostate cancer cells. We provide here the first evidence that Foxy-5 significantly inhibits the initial metastatic dissemination of tumor cells to regional and distal lymph nodes by 90% and 75%, respectively. Importantly, this effect was seen only with the WNT5A-low DU145 cells and not with the WNT5A-high PC3 cells. The inhibiting effect in the DU145-based model occurred despite the fact that no effects were observed on primary tumor growth, apoptosis or proliferation. These findings are consistent with and supported by the in vitro data, where Foxy-5 specifically targets invasion without affecting apoptosis or viability of WNT5A-low prostate cancer cells. To conclude, our data indicate that the WNT5A-mimicking peptide Foxy-5, which has been recently used in a phase 1 clinical trial, is an attractive candidate for complimentary anti-metastatic treatment of prostate cancer patients with tumors exhibiting absent or low WNT5A expression.

Wnt-5a is a synaptogenic factor with neuroprotective properties against Aβ toxicity

Neurodegener Dis 2012;10(1-4):23-6.PMID:22261402DOI:10.1159/000333360.

Background: We have recently found that Wnt-5a regulates the synaptic structure and function in hippocampal neurons. This ligand is expressed in the hippocampus, stimulates dendritic spine morphogenesis and increases glutamatergic neurotransmission. Moreover, we have also shown that Wnt-5a induces the clustering of PSD-95. Objective: To explore the role of Wnt-5a in the formation of synaptic contacts. Methods: Primary rat hippocampal neurons were exposed to a formylated hexapeptide (Foxy-5) derived from the sequence of Wnt-5a to study synapse formation and function. Results: In short-term experiments, Wnt-5a only induced the clustering of PSD-95 but had no effect on the density of presynaptic puncta, while in long-term experiments, it induced both pre- and postsynaptic protein clustering and the number of synaptic contacts, in agreement with electrophysiological studies. In long-term experiments, Foxy-5 increased miniature excitatory postsynaptic current amplitude and frequency. Conclusion: Our findings indicate that Wnt-5a induces synapse formation in hippocampal neurons. In addition, we discuss recent findings indicating a neuroprotective action of Wnt-5a against Aβ neurotoxicity.