1. Metabolic Enzyme/Protease Cytoskeleton
  2. E1/E2/E3 Enzyme Cadherin
  3. Hakin-1

Hakin-1 is a E3 Ubiquitin-Ligase Hakai inhibitor. Hakin-1 blocks Hakai-mediated global ubiquitination and specific ubiquitination of E-cadherin and inhibits epithelial-mesenchymal transition (EMT) progression. Hakan-1 inhibits tumor progression and cancer metastasis. Hakin-1 can be used for the study of carcinoma such as colorectal cancer.

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Hakin-1

Hakin-1 Chemical Structure

CAS No. : 346660-34-2

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Description

Hakin-1 is a E3 Ubiquitin-Ligase Hakai inhibitor. Hakin-1 blocks Hakai-mediated global ubiquitination and specific ubiquitination of E-cadherin and inhibits epithelial-mesenchymal transition (EMT) progression. Hakan-1 inhibits tumor progression and cancer metastasis. Hakin-1 can be used for the study of carcinoma such as colorectal cancer[1].

In Vitro

Hakin-1 (10-3000 μM) exhibits dose-dependent inhibitory effects on the viability of HT-29, LoVo, MDCK, HaKai-MDCK (clone-4) and HaKai-MDCK (clone-11) cells with IC50 of 289.2, 159.1, 265.6, 176.3 and 165.4 μM[1].
Hakin-1 (50-100 μM) promotes the upregulation of E-cadherin and Cortactin, and downregulates Vimentin, but there is no change in mRNA levels in HT-29 cells[1].
Hakin-1 (50-100 μM, 21-28 days) significantly reduces the formation of cancer cell colonies in HT-29 and HaKai-MDCK cells[1].
Hakin-1 (50-100 μM, 48 h) reduces cell invasion and cell migration in HT-29, LoVo and HaKai-MDCK cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Migration Assay [1]

Cell Line: HT-29, LoVo and HaKai-MDCK cells
Concentration: 50 and 100 μM
Incubation Time: 24 h
Result: Strongly inhibits the migratory ability of HT-29 cells.

Cell Invasion Assay[1]

Cell Line: HT-29, LoVo and HaKai-MDCK cells
Concentration: 50 and 100 μM
Incubation Time: 24 h
Result: Strongly inhibits the invasive ability of LoVo cells.
In Vivo

Hakin-1 (5 mg/kg, i.p., 3 times a week for 20 days) reduces tumour growth in Hakai-MDCK tumour xenografts, on which E-cadherin is not expressed, and this effect is accompanied by a reduced expression of N-cadherin mesenchymal marker and reduced formation of lung micrometastases[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Hakai-MDCK induced xenografts model established in six weeks old athymic nu/nu mice[1]
Dosage: 5 mg/kg
Administration: Intraperitoneal injection (i.p.), 3 times a week for 20 days
Result: Inhibited tumor growth and promoted tumor differentiation.
Significantly reduced the number of Ki67-positive cells, which are markers of tumor proliferation, and the mitotic index.
Significantly reduced the density of blood vessels within the tumor (as indicated by CD31 labeling).
Reduced the level of N-cadherin and increased Cortactin.
Significantly reduced pulmonary micrometastases.
No obvious systemic toxicity.
Molecular Weight

385.35

Formula

C16H11N5O5S

CAS No.
SMILES

O=C(C1=CC=C(N2N=NN=C2SCC(C3=CC=C([N+]([O-])=O)C=C3)=O)C=C1)O

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Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Hakin-1
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HY-176861
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