Tarloxotinib bromide, Inhibitor

Tarloxotinib bromide

Cat. Num. AAA5754010

• Purity: 98.00%
• Synonyms: Tarloxotinib bromide; TH-4000; inhibitor

• Purity/Purification: 98.00%
• Form/Format: Solid. Powder

• Solubility: DMSO: 33mg/mL (48.40mM); (<1mg/ml refers to the product slightly soluble or insoluble)
• Formula: C24H24Br2ClN9O3
• SMILES: BrC1=C(Cl)C=CC(NC2=NC=NC3=C2C=C(NC(/C=C/C[N+](C)(C)CC4=C([N+]([O-])=O)N=CN4C)=O)N=C3)=C1.[Br-]
• CAS Number: 1636180-98-7
• Target & IC50: EGFR/HER2
• In Vitro: The prototype WT EGFR-driven xenograft model (A431) was used to "reverse" the plasma exposure of each drug in human subjects reported back to the xenograft model, so that the baseline tallotinib bromide for each EGFR-TKI Activity. Only treatment with clinically relevant doses and schedules of Tarloxotinib bromide is associated with tumor regression and durable inhibition of WT EGFR tumor phosphorylation.Consistent with these findings, tarotinib bromide treatment, can also return the WT EGFR NSCLC tumor models H125 and H1648, proving that tarotinib bromide provides the necessary therapeutic indicators for inhibiting WT EGFR in vivo[1].
• Preparation and Storage: Store at -20 degree C for 3 years powder; -80 degree C for 2 years in solvent

Structure

Related Product Information for Tarloxotinib bromide, inhibitor

Tarloxotinib bromide is an irreversible inhibitor of EGFR/HER2.

Product Categories/Family for Tarloxotinib bromide, inhibitor

Angiogenesis; EGFR; JAK/STAT signaling; Tyrosine Kinase/Adaptors

References

Shevan Silva, Abstract A67: Preclinical efficacy of tarloxotinib bromide (TH-4000), a hypoxia-activated EGFR/HER2 inhibitor: rationale for clinical evaluation in EGFR mutant, T790M-negative NSCLC following progression on EGFR-TKI therapy. Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA.
Shevan Silva, Abstract A67: Preclinical efficacy of tarloxotinib bromide (TH-4000), a hypoxia-activated EGFR/HER2 inhibitor: rationale for clinical evaluation in EGFR mutant, T790M-negative NSCLC following progression on EGFR-TKI therapy. Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA.
Adam V. Patterson, Abstract 5358: The hypoxia-activated EGFR-TKI TH-4000 overcomes erlotinib-resistance in preclinical NSCLC models at plasma levels achieved in a Phase 1 clinical trial. AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA.
Adam V. Patterson, Abstract 5358: The hypoxia-activated EGFR-TKI TH-4000 overcomes erlotinib-resistance in preclinical NSCLC models at plasma levels achieved in a Phase 1 clinical trial. AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA.