In various embodiments a cancer treatment method is provided based on inhibition of proline catabolism. When combined with p53 restoration therapy and/or inhibition of glutaminase, the inhibition of proline catabolism results in a “synthetic lethal” and synergistic anticancer response. Novel suicide inhibitors that induce the degradation of proline dehydrogenase (PRODH) are also provided. Also provided is a method of assaying PRODH to identify responders/non-responders to inhibition of proline catabolism and/or glutaminase.

The present invention relates to a kit for quantitative analysis of glycated hemoglobin (HbA1c), and the kit for quantitative analysis of HbA1c according to the present invention has excellent long-term stability of an enzyme reagent and thus has an effect of easily overcoming the disadvantages of the conventional reagents used in enzyme assays (e.g., storage, accuracy, portability, convenience of use, etc.).

A system for the electrochemical detection of creatinine levels includes a test strip including an electrode and a counter electrode, the electrode and counter electrode located proximate to a sample reception area; and a coating on one of the electrode and counter electrode, the coating including a reagent coating for creatinine.

There is provided a novel quantification method for quantifying a concentration of EAP, which is a biomarker of depression, an enzyme for quantitation, a composition for quantitation, a kit for quantitation or a sensor for quantitation. There is provided a quantification method of ethanolamine phosphate by adding oxidoreductase to a sample containing ethanolamine phosphate. A mediator may be reduced by adding the oxidoreductase, and the reduced mediator may be reacted with a reagent to determine a concentration of ethanolamine phosphate. In addition, hydrogen peroxide produced by adding the oxidase as the oxidoreductase may be reacted with a reagent to determine a concentration of the ethanolamine phosphate.

In various embodiments a cancer treatment method is provided based on inhibition of proline catabolism. When combined with p53 restoration therapy and/or inhibition of glutaminase, the inhibition of proline catabolism results in a synthetic lethal and synergistic anticancer response. Novel suicide inhibitors that induce the degradation of proline dehydrogenase (PRODH) are also provided. Also provided is a method of assaying PRODH to identify responders/non-responders to inhibition of proline catabolism and/or glutaminase.

The present invention relates to a kit for quantitative analysis of glycated hemoglobin (HbA1c), and the kit for quantitative analysis of HbA1c according to the present invention has excellent long-term stability of an enzyme reagent and thus has an effect of easily overcoming the disadvantages of the conventional reagents used in enzyme assays (e.g., storage, accuracy, portability, convenience of use, etc.).