61019-14-5

Usage

Uses

Used in Pharmaceutical Research and Drug Development:
3-Thiophenecarboxamide, 2-amino-5-(4-fluorophenyl)is used as a research compound for the development of new medications, leveraging its unique structure and properties to potentially contribute to novel therapeutic agents.
Used in Chemical Synthesis:
3-Thiophenecarboxamide, 2-amino-5-(4-fluorophenyl)is also used as a building block in the synthesis of more complex chemical compounds, facilitating the creation of a variety of advanced chemical entities for various applications.

Upstream product

• 1736-67-0 4-fluorophenylacetaldehyde 
• 107-91-5 cyanoacetic acid amide 
• 1093877-97-4 benzyl [3-(aminocarbonyl)-5-iodo-2-thienyl]carbamate 
• 1093877-96-3 benzyl [3-(aminocarbonyl)-2-thienyl]carbamate 
• 14080-51-4 2-aminothiophene-3-carboxamide 

Downstream Products

• 507475-17-4 2-(carbamoylamino)-5-(4-fluorophenyl)thiophene-3-carboxamide 
• 1093877-74-7 C₁₇H₁₄FN₃OS 

Relevant academic research and scientific papers

Thiophene carboxamide inhibitors of JAK2 as potential treatments for myleoproliferative neoplasms

A series of carboxamide-substituted thiophenes demonstrating inhibition of JAK2 is described. Development of this chemical series began with the bioisosteric replacement of a urea substituent by a pyridyl ring. Issues of chemical and metabolic stability were solved using the results of both in vitro and in vivo studies, ultimately delivering compounds such as 24 and 25 that performed well in an acute PK/PD model measuring p-STAT5 inhibition.

INHIBITORS OF JANUS KINASES

The instant invention provides for compounds that inhibit the four known mammalian JAK kinases (JAK1, JAK2, JAK3 and TYK2) and PDK1. The invention also provides for compositions comprising such inhibitory compounds and methods of inhibiting the activity of JAK1, JAK2, JAK3, TYK2 and PDK1 by administering the compound to a patient in need of treatment for myeloproliferative disorders or cancer.

INHIBITORS OF JANUS KINASES

The instant invention provides for compounds that inhibit the four known mammalian JAK kinases (JAK1, JAK2, JAK3 and TYK2) and PDK1. The invention also provides for compositions comprising such inhibitory compounds and methods of inhibiting the activity of JAK1, JAK2, JAK3 TYK2 and PDK1 by administering the compound to a patient in need of treatment for myeloproliferative disorders or cancer.

Nf-kb inhibitors

The present invention provides a specific compound and methods for treating diseases related to the inhibition of IKK-β phosphorylation of IK.

Attenuation of murine collagen-induced arthritis by a novel, potent, selective small molecule inhibitor of IκB kinase 2, TPCA-1 (2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide), occurs via reduction of proinflammatory cytokines and antigen-induced T cell proliferation

Demonstration that IκB kinase 2 (IKK-2) plays a pivotal role in the nuclear factor-κB-regulated production of proinflammatory molecules by stimuli such as tumor necrosis factor (TNF)-α and interleukin (IL)-1 suggests that inhibition of IKK-2 may be beneficial in the treatment of rheumatoid arthritis. In the present study, we demonstrate that a novel, potent (IC50 = 17.9 nM), and selective inhibitor of human IKK-2, 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide (TPCA-1), inhibits lipopolysaccharide-induced human monocyte production of TNF-α, IL-6, and IL-8 with an IC50 = 170 to 320 nM. Prophylactic administration of TPCA-1 at 3, 10, or 20 mg/kg, i.p., b.i.d., resulted in a dose-dependent reduction in the severity of murine collagen-induced arthritis (CIA). The significantly reduced disease severity and delay of disease onset resulting from administration of TPCA-1 at 10 mg/kg, i.p., b.i.d. were comparable to the effects of the antirheumatic drug, etanercept, when administered prophylactically at 4 mg/kg, i.p., every other day. Nuclear localization of p65, as well as levels of IL-1β, IL-6, TNF-α, and interferon-γ, were significantly reduced in the paw tissue of TPCA-1- and etanercept-treated mice. In addition, administration of TPCA-1 in vivo resulted in significantly decreased collagen-induced T cell proliferation ex vivo. Therapeutic administration of TPCA-1 at 20 mg/kg, but not at 3 or 10 mg/kg, i.p., b.i.d., significantly reduced the severity of CIA, as did etanercept administration at 12.5 mg/kg, i.p., every other day. These results suggest that reduction of proinflammatory mediators and inhibition of antigen-induced T cell proliferation are mechanisms underlying the attenuation of CIA by the IKK-2 inhibitor, TPCA-1.

Nf-kb inhibitors

The present invention provides novel compounds and methods for treating diseases with aminothiophene inhibitors of IKK-β phosphorylation of IκB.

Thiophene derivatives

Compounds of the formula: SPC1 Wherein R1 is NHR5 or OR5 where R5 is a hydrogen atom or alkyl group of 1-6 carbon atoms; R2 is a hydrogen atom or a CO.R6 group where R6 is an alk