The attempt to synthesize a
lipid A-like component (the active portion of
lipopolysaccharides, but lacking its endotoxic activity) resulted in the production of fatty acyl
sugars of which
maltose tetrapalmitate was seen to yield the most promising results. It shows no endotoxic activity and elicits an antitumor response in
tumor-transplanted animals as shown by (a) an enhancement of the host's capacity to reject a large number of
tumor cells, (b) retardation of growth in
tumor size, and (c) induction of hemorrhagic
necrosis in certain
tumors. Experiments with mammary
ascites carcinoma show
maltose tetrapalmitate to be as effective as is bacterial
glycolipid mR595 in its antitumor activity. The degree of sensitivity to
maltose tetrapalmitate varies with the
tumor-host system: mammary
ascites carcinoma less than NH = Cl2TSV5S = B16 less than L26. The mode of action of
maltose tetrapalmitate appears to be via its modulation of the immune system. It is itself noncytotoxic to
tumor cells in vitro. It is seen to stimulate the spleen cells of certain animals mitogenically, although it causes
tumor rejection in all the types of animals tested. Also, it activates peritoneal exudate macrophages in
tumor-bearing animals; whether specifically or nonspecifically has not yet been established.