AIM 100

Pricing Availability Delivery Time Qty
Cat.No. 4946 - AIM 100 | C23H21N3O2 | CAS No. 873305-35-2
Description: Potent and selective Ack1 (TNK2) inhibitor
Chemical Name: 5,6-Diphenyl-N-[[(2S)-tetrahydro-2-furanyl]methyl]furo[2,3-d]pyrimidin-4-amine
Purity: ≥98% (HPLC)
Datasheet
Citations
Literature

Biological Activity

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.

Compound Libraries

AIM 100 is also offered as part of the Tocriscreen Plus and Tocriscreen Kinase Inhibitor Toolbox II. Find out more about compound libraries available from Tocris.

Technical Data

M. Wt 371.43
Formula C23H21N3O2
Storage Store at +4°C
Purity ≥98% (HPLC)
CAS Number 873305-35-2
PubChem ID 11501591
InChI Key XNFHHOXCDUAYSR-SFHVURJKSA-N
Smiles C1(C(C4=CC=CC=C4)=C(C5=CC=CC=C5)O3)=C3N=CN=C1NC[C@H]2OCCC2

The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.

All Tocris products are intended for laboratory research use only.

Solubility Data

Solvent Max Conc. mg/mL Max Conc. mM
Solubility
DMSO 37.14 100
ethanol 37.14 100

Preparing Stock Solutions

The following data is based on the product molecular weight 371.43. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.

Select a batch to recalculate based on the batch molecular weight:
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

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Reconstitution Calculator

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Product Datasheets

Safety Datasheet

References

References are publications that support the products' biological activity.

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


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Keywords: AIM 100, supplier, AIM100, ack1, inhibitors, inhibits, selective, kinases, TNK2, tyrosine, kinase, non-receptor, Androgen, Receptor, Ack1, Ack1, Tocris Bioscience

Citations for AIM 100

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Literature in this Area

Cancer

Cancer Research Product Guide

A collection of over 750 products for cancer research, the guide includes research tools for the study of:

  • Cancer Metabolism
  • Epigenetics in Cancer
  • Receptor Signaling
  • Cell Cycle and DNA Damage Repair
  • Angiogenesis
  • Invasion and Metastasis
Kinases

Kinases Product Listing

A collection of over 400 products for kinase research, the listing includes inhibitors of:

  • Receptor Tyrosine Kinases
  • Protein Kinases A, C, D and G
  • PI-3 Kinase, Akt and mTOR
  • MAPK Signaling
  • Receptor Serine/Threonine Kinases
Epigenetics

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

Cancer Metabolism Poster

Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the main targets for cancer metabolism researchers. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways. These distinct metabolic circuits could provide viable cancer therapeutic targets.

Epigenetics in Cancer

Epigenetics in Cancer Poster

Adapted from the 2015 Cancer Product Guide Edition 3, 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.

Pathways for AIM 100

Protocols

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