Abstract: The present invention includes a high throughput screen for an active agent for the treatment of comprising: plating cells at least one pathophysiologically relevant mislocated mutant form of a peroxisomal enzyme; adding a control and compound to each plate from a library of compounds; fixing the cells; contacting the cells with an agent that detects the mislocated mutant form of a peroxisomal enzyme; and imaging the cells in the wells.

Abstract: This application relates to methods of identifying pharmacoperone agents that can restore function to a misfolded protein, such as a misfolded protein that causes disease. Also disclosed are methods of using such pharmacoperone agents to treat a disease or disorder that results from the misfolded protein.

Abstract: This application relates to methods of identifying pharmacoperone agents that can restore function to a misfolded protein, such as a misfolded protein that causes disease. Also disclosed are methods of using such pharmacoperone agents to treat a disease or disorder that results from the misfolded protein.

Abstract: Herein disclosed is a method of rescuing gonadotropin-releasing hormone receptor (GnRHR) mutants with IN3 or a mimetic thereof. IN3 significantly rescues 11 missense mutations as assessed by radioligand binding and by IP production. Such rescue occurred despite widely disparate loci along the receptor. In addition, many altered GnRH receptors (terminally truncated, internal deletions, or lacking the ability to form bridges to form tertiary structure) were rescued with IN3.

Abstract: Herein disclosed is a method of rescuing gonadotropin-releasing hormone receptor (GnRHR) mutants with IN3 or a mimetic thereof. IN3 significantly rescues 11 missense mutations as assessed by radioligand binding and by IP production. Such rescue occurred despite widely disparate loci along the receptor. In addition, many altered GnRH receptors (terminally truncated, internal deletions, or lacking the ability to form bridges to form tertiary structure) were rescued with IN3.

Abstract: Herein disclosed is a method of rescuing gonadotropin-releasing hormone receptor (GnRHR) mutants with IN3 or a mimetic thereof. IN3 significantly rescues 11 missense mutations as assessed by radioligand binding and by IP production. Such rescue occurred despite widely disparate loci along the receptor. In addition, many altered GnRH receptors (terminally truncated, internal deletions, or lacking the ability to form bridges to form tertiary structure) were rescued with IN3.

Abstract: A synthetic hormone complex comprising means for binding to the surface of a cell and means for altering second messenger mobilization by the cell. One form of the synthetic hormone complex functions as an antagonist with specific binding affinity for a cell receptor, said hormone in combination with a calcium ion channel inhibitor. Another synthetic hormone complex functioning as an Agonist comprising two or more molecules of a hormone having specific binding affinity for a cell receptor wherein a spacer binding the hormones is 10 to 300 angstroms in length. A method of regulating hormones or other regulatory factors comprising contacting a synthetic hormone complex with a cell surface or internal receptor thereby altering the incorporation of second messenger molecules thereby regulating the physiological function of the cell.