The structure and concentration of sterol in a lipid-defined artificial medium affected the development of the entomogenous nematode, Steinernema feltiae (= Neoaplectana carpocapsae). The nematode grew normally in vitro when the medium was supplemented with Δ 5-desalkylsterol (cholesterol) or Δ 5-desalkylsteryl ester (cholesterol oleate). The minimum amount of cholesterol in the medium that was necessary to support the development of S. feltiae to the climax population (i.e., dauer stage) was 0.0025%. The nematode also completed its life cycle normally when Δ 0- or Δ 7-desalkylsterols (cholestanol and lathosterol) were substituted for cholesterol. In contrast, development was inhibited when the medium contained Δ 5,7-desalkylsterol (7-dehydrocholesterol); however, the nematode population reached the climax stage, in medium containing this sterol, when cholesterol was also present. S. feltiae was able to utilize Δ 5- and Δ 0-24α-ethylsterols (sitosterol and sitostanol) as dietary sterols; however, when a Δ 22-bond was introduced into the side chain (stigmasterol) the rate of development of the nematode slowed significantly. The growth of the nematode was also retarded when the medium contained Δ 5,7,22-24β-methylsterol (ergosterol). The nematode population reached the climax stage in medium containing Δ 8,24-4,4,14α-trimethylsterol (lanosterol) only when cholesterol was also present. When S. feltiae was exposed to certain hypolipidemic agents, which are known to lower the level of lipids in human plasma (clofibrate, cholestyramine resin, niacin, and d-thyroxine), all but d-thyroxine affected the growth and development of the nematode in vivo (in Heliothis zea) and/or in vitro. Therefore further studies are warranted to determine how these drugs affect the lipid biochemistry of this nematode.