Medullipin I causes a delayed onset depressor response when injected intravenously into rats. The glyceryl compounds selachyl alcohol (SA) and monoolein (MO) cause similar vasodepression. The neutral lipid 1-O-hexadecyl-2-acetyl-sn-glycerol (HAG) was suggested by Blank et al to be medullipin I (Med I, formerly ANRL). Biologic comparisons were made between Med I and various glyceryl compounds, including SA, MO, HAG, alkyl glyceryl ethers of phosphatidyl choline (termed APRL by us), diacylated SA, and the n-butyl boronic acid derivative of SA and MO. The n-butyl boronic acid derivative of Med I also was evaluated. The delay in onset of the depressor response to Med I was reduced by the injection of Med I into the portal vein; that of SA and MO was not. Med I, SA, and MO were activated by the liver, while APRL and HAG were not. Tween 20 inhibited Med I, SA, and MO, but not APRL and HAG. Proadifen (SKF 525A) inhibited Med I, but not SA and MO. The n-butyl boronic acid derivatives of SA, MO, and Med I were inactive. Med I, like SA and MO, appeared to have two hydroxyl groups in close proximity. It was concluded that Med I is neither HAG, APRL, SA, nor MO.