AtheroGenics Inc., a Georgia start-up company, raised nearly $10million in a third round of financing to support its development oforal compounds to treat the underlying molecular mechanismsinvolved in atherosclerosis, or hardening of the arteries.

Russell Medford, president and CEO of AtheroGenics, said theNorcross-based company expects to begin a Phase I trial in Europewith its lead drug candidate in the first quarter of 1997.

The small-molecule compound, AGI-H1, is described as a vascularprotectant and is designed to block the inflammatory response thatcauses arteries to thicken with the growth of atherosclerotic plaques,which can rupture and form blood clots.

"We identified a signal transduction pathway that regulates theinflammatory response genes associated with atherosclerosis," saidMedford, referring to research he conducted with AtheroGenics' co-founder, Wayne Alexander, at Emory University School of Medicinein Atlanta.

Medford is an associate professor of cardiology and director of theMolecular Cardiology Research Center at Emory. Alexander is aprofessor at Emory and chief of cardiology at Emory UniversityHospital. AtheroGenics, formed in 1994, has 13 employees.

Medford said the third financing round, which generated $9.3million, gives the company a total of $14 million raised in two years.The Sprout Group, of New York, and Domain Partners, of Princeton,N.J., led the current investor group. AtheroGenics received seedfinancing in 1994 from Alliance Technology Ventures of Atlanta.Participating in the second round of fund raising last year wereSanderling, of Menlo Park, Calif., and New York Life InsuranceVentures, of New York.

Current treatments for atherosclerosis, Medford said, primarilyinvolve controlling risk factors, such as high cholesterol, high bloodpressure, obesity and smoking, which can trigger an improperinflammatory response.

In addition to AGI-H1, AtheroGenics has another oral drug underdevelopment, called AGI-H15. Both are designed to block theinflammatory assault regardless of external stresses on the arteries.

Medford said the company's small-molecule compounds target cell-signaling pathways for two gene sets in vascular endothelial cells,which line the inner surface of blood vessels. The genes expressvascular cell adhesion molecule-1 (VCAM-1) and monocytechemoattractant protein-1 (MCP-1).

The company's researchers have stated the drug candidates "havedemonstrated an ability to suppress macrophage recruitment to thearterial wall and to suppress aortic endothelial VCAM-1 expression."n

-- Charles Craig

(c) 1997 American Health Consultants. All rights reserved.