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Potent CXCR4 antagonist (IC50 = 1.1 nM in calcium mobilization assays). Orally available. Blocks interaction with the HIV envelope protein, gp120 (IC50 = 7 nM, inhibition of X4-tropic HIV-1IIIB attachment).
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 479.57. 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||2.09 mL||10.43 mL||20.85 mL|
|5 mM||0.42 mL||2.09 mL||4.17 mL|
|10 mM||0.21 mL||1.04 mL||2.09 mL|
|50 mM||0.04 mL||0.21 mL||0.42 mL|
References are publications that support the biological activity of the product.
Thoma et al (2008) Orally bioavailable isothioureas block function of the chemokine receptor CXCR4 in vitro and in vivo. J.Med.Chem. 51 7915 PMID: 19053768
If you know of a relevant reference for IT1t dihydrochloride, please let us know.
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Keywords: IT1t dihydrochloride, IT1t dihydrochloride supplier, CXCR4, antagonists, HIV, envelope, protein, gp120, chemokines, receptors, type, 4, Antivirals, Chemokine, CXC, Receptors, 4596, Tocris Bioscience
2 Citations for IT1t dihydrochloride
Citations are publications that use Tocris products. Selected citations for IT1t dihydrochloride include:
White et al (2020) CRISPR-Mediated Protein Tagging with Nanoluciferase to Investigate Native Chemokine Receptor Function and Conformational Changes. Cell Chem Bio PMID: 32053779
Smith et al (2019) Control of TLR7-mediated type I IFN signaling in pDCs through CXCR4 engagement-A new target for lupus treatment. Sci Adv 5 eaav9019 PMID: 31309143
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Literature in this Area
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Rheumatoid Arthritis Poster
Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.