1307310-01-5

Upstream product

• 108-85-0 1-bromocyclohexane 
• 64217-99-8 1-(3-vinylphenyl)ethan-1-one 
• 695-12-5 vinylcyclohexane 
• 2142-63-4 1-(3-Bromophenyl)ethanone 

Downstream Products

• 1307310-15-1 C₂₄H₂₅NO₂S 
• 1307310-02-6 2-bromo-1-(3-(2-cyclohexylethyl)phenyl)ethanone 
• 1307310-03-7 tert-butyl (2-(3-(2-cyclohexylethyl)phenyl)-2-oxoethyl)terephthalate 
• 1307310-08-2 4-(4-(3-(2-cyclohexylethyl)phenyl)oxazol-2-yl)benzoic acid 
• 1307310-09-3 (S)-1-(4-(4-(3-(2-cyclohexylethyl)phenyl)oxazol-2-yl)benzoyl)pyrrolidine-2-carbonitrile 
• 1307310-10-6 (S)-1-(4-(4-(3-(2-cyclohexylethyl)phenyl)oxazol-2-yl)benzoyl)pyrrolidine-2-carboximidamide hydrochloride 
• 1307310-13-9 tert-butyl 4-(4-(3-(2-cyclohexylethyl)phenyl)thiazol-2-yl)benzoate 
• 1307310-14-0 (S)-1-(4-(4-(3-(2-cyclohexylethyl)phenyl)thiazol-2-yl)benzoyl)pyrrolidine-2-carbonitrile 
• 1307310-16-2 (S)-1-(4-(4-(3-(2-cyclohexylethyl)phenyl)thiazol-2-yl)benzoyl)pyrrolidine-2-carboximidamide hydrochloride 

Relevant academic research and scientific papers

Fe-Catalyzed Reductive Couplings of Terminal (Hetero)Aryl Alkenes and Alkyl Halides under Aqueous Micellar Conditions

The combination of a vinyl-substituted aromatic or heteroaromatic and an alkyl bromide or iodide leads, in the presence of Zn and a catalytic amount of an Fe(II) salt, to a net reductive coupling. The new C-C bond is regiospecifically formed at rt at the β-site of the alkene. The coupling only occurs in an aqueous micellar medium, where a radical process is likely, supported by several control experiments. A mechanism based on these data is proposed.

Development of amidine-based sphingosine kinase 1 nanomolar inhibitors and reduction of sphingosine 1-phosphate in human leukemia cells

Sphingosine 1-phosphate (S1P) is a bioactive lipid that has been identified as an accelerant of cancer progression. The sphingosine kinases (SphKs) are the sole producers of S1P, and thus, SphK inhibitors may prove effective in cancer mitigation and chemosensitization. Of the two SphKs, SphK1 overexpression has been observed in a myriad of cancer cell lines and tissues and has been recognized as the presumptive target over that of the poorly characterized SphK2. Herein, we present the design and synthesis of amidine-based nanomolar SphK1 subtype-selective inhibitors. A homology model of SphK1, trained with this library of amidine inhibitors, was then used to predict the activity of additional, more potent, inhibitors. Lastly, select amidine inhibitors were validated in human leukemia U937 cells, where they significantly reduced endogenous S1P levels at nanomolar concentrations.