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Biological Activity for AIM 100
AIM 100 is a potent Ack1 (TNK2) inhibitor (IC50 = 22 nM). Exhibits selectivity for Ack1 over ABL1, BTK, Lck and LYN; exhibits no inhibition of 25 other kinases. Suppresses phosphorylation of Tyr267 of the androgen receptor in prostate cancer cells. Also suppresses growth of radioresistant castration-resistant prostate cancer in xenograft tumors in mice. Also promotes DAT endocytosis and oligomerization.
Compound Libraries for AIM 100
Technical Data for AIM 100
|Storage||Store at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for AIM 100
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for AIM 100
The following data is based on the product molecular weight 371.43. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.69 mL||13.46 mL||26.92 mL|
|5 mM||0.54 mL||2.69 mL||5.38 mL|
|10 mM||0.27 mL||1.35 mL||2.69 mL|
|50 mM||0.05 mL||0.27 mL||0.54 mL|
References for AIM 100
References are publications that support the biological activity of the product.
Mahajan et al (2012) Ack1-mediated androgen receptor phosphorylation modulates radiation resistance in castration-resistant prostate cancer. J.Biol.Chem. 287 22112 PMID: 22566699
Mahajan et al (2010) Effect of Ack1 tyrosine kinase inhibitor on ligand-independent androgen receptor activity. Prostate 70 1274 PMID: 20623637
Sorkina et al (2018) Small molecule induced oligomerization, clustering and clathrin-independent endocytosis of the dopamine transporter. Elife. 7 PMID: 29630493
If you know of a relevant reference for AIM 100, please let us know.
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Keywords: AIM 100, AIM 100 supplier, AIM100, ack1, inhibitors, inhibits, selective, kinases, TNK2, tyrosine, kinase, non-receptor, Androgen, Receptor, Ack1, Dopamine, Transporters, 4946, Tocris Bioscience
2 Citations for AIM 100
Citations are publications that use Tocris products. Selected citations for AIM 100 include:
Guy A et al (2022) Systemic RNA Interference Defective (SID) genes modulate dopaminergic neurodegeneration in C. elegans. PLoS Genet 18 e1010115 PMID: 35984862
Verduzco et al (2018) Ceritinib Enhances the Efficacy of Trametinib in BRAF/NRAS-Wild-Type Melanoma Cell Lines. Mol Cancer Ther 17 73 PMID: 29133622
Do you know of a great paper that uses AIM 100 from Tocris? Please let us know.
Reviews for AIM 100
Average Rating: 5 (Based on 1 Review.)
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Combined pharmacological inhibition of MEK and ACK1 suppresses long-term growth of WM209 and SK-MEL-23 cells.
Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Epigenetics Scientific Review
Written by Susanne Müller-Knapp and Peter J. Brown, this review gives an overview of the development of chemical probes for epigenetic targets, as well as the impact of these tool compounds being made available to the scientific community. In addition, their biological effects are also discussed. Epigenetic compounds available from Tocris are listed.
Cancer Metabolism Poster
This poster summarizes the main metabolic pathways in cancer cells and highlights potential targets for cancer therapeutics. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways providing potential cancer therapeutic targets.
Epigenetics in Cancer PosterUpdated
This poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.