R. Kodela

发表

Synthesis and anti-cancer potential of the positional isomers of NOSH-aspirin (NBS-1120) a dual nitric oxide and hydrogen sulfide releasing hybrid.

K. Kashfi, M. Chattopadhyay, Federica Vannini, 2015, Bioorganic & medicinal chemistry letters.

NOSH-aspirin (NBS-1120), a novel nitric oxide- and hydrogen sulfide-releasing hybrid has enhanced chemo-preventive properties compared to aspirin, is gastrointestinal safe with all the classic therapeutic indications.

K. Kashfi, M. Chattopadhyay, C. Velázquez-Martínez, 2015, Biochemical pharmacology.

Positional isomerism markedly affects the growth inhibition of colon cancer cells by NOSH-aspirin: COX inhibition and modeling☆

K. Kashfi, M. Chattopadhyay, P. Rao, 2015, Redox biology.

14,15-Epoxyeicosa-5,8,11-trienoic acid (14,15-EET) surrogates containing epoxide bioisosteres: influence upon vascular relaxation and soluble epoxide hydrolase inhibition.

J. Falck, B. Hammock, J. Falck, 2009, Journal of medicinal chemistry.

Cardioprotective effect of a dual acting epoxyeicosatrienoic acid analogue towards ischaemia reperfusion injury

J. Falck, J. Seubert, K. Chaudhary, 2011, British journal of pharmacology.

Hydrogen sulfide-releasing aspirin inhibits the growth of leukemic Jurkat cells and modulates β-catenin expression.

K. Kashfi, N. Nath, S. Metkar, 2013, Leukemia research.

Hydrogen sulfide-releasing aspirin modulates xenobiotic metabolizing enzymes in vitro and in vivo.

K. Kashfi, N. Nath, M. Chattopadhyay, 2012, Biochemical pharmacology.

NOSH-Aspirin: A Novel Nitric Oxide-Hydrogen Sulfide-Releasing Hybrid: A New Class of Anti-inflammatory Pharmaceuticals.

K. Kashfi, M. Chattopadhyay, R. Kodela, 2012, ACS medicinal chemistry letters.

Positional Isomers of Aspirin Are Equally Potent in Inhibiting Colon Cancer Cell Growth: Differences in Mode of Cyclooxygenase Inhibition

K. Kashfi, M. Chattopadhyay, S. Goswami, 2013, The Journal of Pharmacology and Experimental Therapeutics.

NOSH-aspirin (NBS-1120) inhibits pancreatic cancer cell growth in a xenograft mouse model: Modulation of FoxM1, p53, NF-κB, iNOS, caspase-3 and ROS.

K. Kashfi, N. Nath, M. Chattopadhyay, 2020, Biochemical pharmacology.

NOSH-sulindac (AVT-18A) is a novel nitric oxide- and hydrogen sulfide-releasing hybrid that is gastrointestinal safe and has potent anti-inflammatory, analgesic, antipyretic, anti-platelet, and anti-cancer properties

K. Kashfi, M. Chattopadhyay, R. Kodela, 2015, Redox biology.

Synthesis and biological activity of NOSH-naproxen (AVT-219) and NOSH-sulindac (AVT-18A) as potent anti-inflammatory agents with chemotherapeutic potential.

K. Kashfi, M. Chattopadhyay, R. Kodela, 2013, MedChemComm.

P09 Therapeutic potential of NOSH-aspirin, a dual nitric oxide- and hydrogen sulfide-donating hybrid in colon cancer

K. Kashfi, M. Chattopadhyay, R. Kodela, 2013 .

NOSH‐aspirin a dual nitric oxide‐and hydrogen sulfide‐releasing hybrid reciprocally regulates NF‐κB: S‐nitrosylation vs S‐sulfhydration

K. Kashfi, M. Chattopadhyay, R. Kodela, 2013 .

Hydrogen sulfide-releasing aspirin suppresses NF-κB signaling in estrogen receptor negative breast cancer cells in vitro and in vivo.

A. Barsegian, K. Kashfi, N. Nath, 2012, Biochemical pharmacology.

Abstract 4608: Hydrogen sulfide-releasing aspirin inhibits the growth of leukemic Jurkat cells and modulates β-catenin expression

K. Kashfi, J. Crowell, M. Chattopadhyay, 2011 .

Modulation of stress genes expression profile by nitric oxide-releasing aspirin in Jurkat T leukemia cells.

K. Kashfi, N. Nath, J. Crowell, 2010, Biochemical pharmacology.

Nitric Oxide-Releasing Aspirin Suppresses NF-κB Signaling in Estrogen Receptor Negative Breast Cancer Cells in Vitro and in Vivo

K. Kashfi, N. Nath, M. Chattopadhyay, 2015, Molecules.

Gastrointestinal safety, chemotherapeutic potential, and classic pharmacological profile of NOSH‐naproxen (AVT‐219) a dual NO‐ and H2S‐releasing hybrid

K. Kashfi, M. Chattopadhyay, R. Kodela, 2016, Pharmacology research & perspectives.

Hydrogen sulfide-releasing naproxen suppresses colon cancer cell growth and inhibits NF-κB signaling

K. Kashfi, N. Nath, M. Chattopadhyay, 2015, Drug design, development and therapy.

NOSH-Aspirin Inhibits Colon Cancer Cell Growth: Effects Of Positional Isomerism.

K. Kashfi, M. Chattopadhyay, Federica Vannini, 2015, Redox biology.

JS-K, a nitric oxide-releasing prodrug, modulates ß-catenin/TCF signaling in leukemic Jurkat cells: evidence of an S-nitrosylated mechanism.

K. Kashfi, N. Nath, J. Saavedra, 2010, Biochemical pharmacology.

NOSH‐aspirin (NBS‐1120), a novel nitric oxide and hydrogen sulfide releasing hybrid, attenuates neuroinflammation induced by microglial and astrocytic activation: A new candidate for treatment of neurodegenerative disorders

P. Mcgeer, E. Mcgeer, Moonhee Lee, 2013, Glia.

NOSH-aspirin (NBS-1120), a novel nitric oxide- and hydrogen sulfide-releasing hybrid is a potent inhibitor of colon cancer cell growth in vitro and in a xenograft mouse model.

K. Kashfi, K. Olson, M. Chattopadhyay, 2012, Biochemical and biophysical research communications.

Hydrogen sulfide-releasing NSAIDs inhibit the growth of human cancer cells: a general property and evidence of a tissue type-independent effect.

K. Kashfi, N. Nath, M. Chattopadhyay, 2012, Biochemical pharmacology.

NO-releasing NSAIDs suppress NF-κB signaling in vitro and in vivo through S-nitrosylation.

K. Kashfi, J. Crowell, M. Chattopadhyay, 2010, Cancer letters.

Abstract 4793: NOSH-aspirin inhibits breast cancer cell growth: an effect modulated through reactive oxygen species and independent of the ER status.

K. Kashfi, N. Nath, M. Chattopadhyay, 2013 .

Synthesis and biological activity of acetyl-protected hydroxybenzyl diethyl phosphates (EHBP) as potential chemotherapeutic agents.

K. Kashfi, N. Nath, J. Crowell, 2011, Bioorganic & medicinal chemistry letters.

14,15-Epoxyeicosa-5,8,11-trienoic acid (14,15-EET) surrogates containing epoxide bioisosteres: influence upon vascular relaxation and soluble epoxide hydrolase inhibition.

B. Hammock, J. Capdevila, W. Campbell, 2009, Journal of medicinal chemistry.