Experience

InnoSense

• Chemical Manufacturing
• 1 - 100 Employee

• Associate Director

  • Apr 2022 - Present



UCLA

• United States
• Higher Education
• 700 & Above Employee

• Assistant Project Scientist

  • May 2016 - Apr 2022

  Cancer immunotherapy for lung cancer Cancer immunotherapy for lung cancer



University of Southern California

• United States
• Higher Education
• 700 & Above Employee

• Research Associate

  • Jul 2014 - Oct 2015

  Characterized the role of Dlk1 in liver regeneration, wound healing, and liver cancer using mouse models and primary liver parenchyma and non-parenchymal cell lines. Searched for the elusive receptor for the Dlk1 ligand through knocking down genes of interest in immortalized and primary cell lines using adenovirus and lentivirus techniques. Validated the genes of interests with immunoprecipitation, immunohistochemisty, biochemical assays (i.e. ELISA and BrdU), and RT-qPCR. Created… Show more Characterized the role of Dlk1 in liver regeneration, wound healing, and liver cancer using mouse models and primary liver parenchyma and non-parenchymal cell lines. Searched for the elusive receptor for the Dlk1 ligand through knocking down genes of interest in immortalized and primary cell lines using adenovirus and lentivirus techniques. Validated the genes of interests with immunoprecipitation, immunohistochemisty, biochemical assays (i.e. ELISA and BrdU), and RT-qPCR. Created transgenic mice colonies using Cre-LoxP and Crispr-CAS systems. Co-authored an invited review paper on the role of morphogens as therapeutics in liver fibrosis. Show less Characterized the role of Dlk1 in liver regeneration, wound healing, and liver cancer using mouse models and primary liver parenchyma and non-parenchymal cell lines. Searched for the elusive receptor for the Dlk1 ligand through knocking down genes of interest in immortalized and primary cell lines using adenovirus and lentivirus techniques. Validated the genes of interests with immunoprecipitation, immunohistochemisty, biochemical assays (i.e. ELISA and BrdU), and RT-qPCR. Created… Show more Characterized the role of Dlk1 in liver regeneration, wound healing, and liver cancer using mouse models and primary liver parenchyma and non-parenchymal cell lines. Searched for the elusive receptor for the Dlk1 ligand through knocking down genes of interest in immortalized and primary cell lines using adenovirus and lentivirus techniques. Validated the genes of interests with immunoprecipitation, immunohistochemisty, biochemical assays (i.e. ELISA and BrdU), and RT-qPCR. Created transgenic mice colonies using Cre-LoxP and Crispr-CAS systems. Co-authored an invited review paper on the role of morphogens as therapeutics in liver fibrosis. Show less



UCLA

• United States
• Higher Education
• 700 & Above Employee

• Project Scientist

  • Jul 2013 - Jun 2014

  Examining novel therapeutic interventions for anemia of chronic inflammation in a mouse model that was previously characterized during my postdoctoral years. Managing a high throughput screen for small molecules as potential therapies for iron overload disorders such as hereditary hemachromatosis and beta thalassemia. Collaborating with several chemistry groups to characterized the structural properties of hepcidin. Examining novel therapeutic interventions for anemia of chronic inflammation in a mouse model that was previously characterized during my postdoctoral years. Managing a high throughput screen for small molecules as potential therapies for iron overload disorders such as hereditary hemachromatosis and beta thalassemia. Collaborating with several chemistry groups to characterized the structural properties of hepcidin.



UCLA Health

• United States
• Hospitals and Health Care
• 700 & Above Employee

• Postdoctoral Fellow

  • Jul 2007 - Jul 2013

  Developed and implemented a cell-based high throughput screen to identify small molecules to antagonize the actions of hepcidin, the principal regulator of iron homeostasis. Identified a thiol-reactive compound, fursultiamine, as a hepcidin antagonist. Through cell-based functional assays and radiolabeled-hepcidin binding studies, fursultiamine acts as a hepcidin antagonist by blocking hepcidin from binding to the hepcidin binding domain (HBD) on ferroportin, the receptor for hepcidin and the… Show more Developed and implemented a cell-based high throughput screen to identify small molecules to antagonize the actions of hepcidin, the principal regulator of iron homeostasis. Identified a thiol-reactive compound, fursultiamine, as a hepcidin antagonist. Through cell-based functional assays and radiolabeled-hepcidin binding studies, fursultiamine acts as a hepcidin antagonist by blocking hepcidin from binding to the hepcidin binding domain (HBD) on ferroportin, the receptor for hepcidin and the sole mammalian iron efflux channel. In addition, I am one of the lead authors which details the characterization of the mouse model of anemia of inflammation (also known as anemia of chronic disease). Show less Developed and implemented a cell-based high throughput screen to identify small molecules to antagonize the actions of hepcidin, the principal regulator of iron homeostasis. Identified a thiol-reactive compound, fursultiamine, as a hepcidin antagonist. Through cell-based functional assays and radiolabeled-hepcidin binding studies, fursultiamine acts as a hepcidin antagonist by blocking hepcidin from binding to the hepcidin binding domain (HBD) on ferroportin, the receptor for hepcidin and the… Show more Developed and implemented a cell-based high throughput screen to identify small molecules to antagonize the actions of hepcidin, the principal regulator of iron homeostasis. Identified a thiol-reactive compound, fursultiamine, as a hepcidin antagonist. Through cell-based functional assays and radiolabeled-hepcidin binding studies, fursultiamine acts as a hepcidin antagonist by blocking hepcidin from binding to the hepcidin binding domain (HBD) on ferroportin, the receptor for hepcidin and the sole mammalian iron efflux channel. In addition, I am one of the lead authors which details the characterization of the mouse model of anemia of inflammation (also known as anemia of chronic disease). Show less



Caltech

• United States
• Research Services
• 700 & Above Employee

• Technical Assistant II

  • Feb 2001 - Sep 2001

  Conducted research in Alliance for Cell Signaling (AfCS), multi-disciplinary, multi-institutional consortium to study cellular signaling systems. Specifically, I was part of the Molecular Biology Group to subclone genes in the signaling pathways of two cell types: B lymphocyte and cardiac myocyte. Conducted research in Alliance for Cell Signaling (AfCS), multi-disciplinary, multi-institutional consortium to study cellular signaling systems. Specifically, I was part of the Molecular Biology Group to subclone genes in the signaling pathways of two cell types: B lymphocyte and cardiac myocyte.