Omega-Methylpridoxal, Omega-methylpyridoxamine and omega-methylpyridoxine support growth of rats for several weeks following deletion of vitamin B6 from the ration. Eventually, however, the growth rate in the presence of these compounds slows, and becomes equal to or less than that of vitamin Bg-deficient control animals. The period of growth promotion is decreased greatly when compounds are administered to depleted rats. Following this period of growth-promotion, growth with high concentrations of omega-methylpyridoxine is distinctly less than in control animals; and death results well before any deaths are noted in the control group. In uncomplicated vitamin B6 deficiency on this ration convulsive seizures are infrequent and were observed only following approximately 6 weeks on the deficient diet In contrast, in the animals fed the omega-methyl-analogues of vitamin B6 convulsions occurred frequently, in all animals, starting about 2 weeks after supplementation while substantial weight gains were still occurring. All symptoms were prevented by feeding pyridoxal together with analogues. Following administration of omega-methylpyridoxine to animals, omega-methyl-4-pyridoxic acid appears in the urine in amounts similar to those found for 4-pyridoxic acid following pyridoxine administration. Glutamic-aspartic transaminase and thionase are reduced in omega-methylpyridoxine-fed animals to about the levels found during uncomplicated vitamin B6 deficiency. Correspondingly, omega-methylpyridoxal phosphate was only about 11% as active as pyridoxal phosphate in activating the glutamic-aspartic transaminase, and did not fully activate liver thionase at any concentration. The facts that feeding these analogues first promotes, but eventually inhibits growth, and produces a deficiency of a different type than that found in uncomplicated vitamin B6-deficiency, may be interpreted in terms of (a) the dual character of omega-methylpyridoxal phosphate as an activator for some vitamin B6-dependent enzymes, but not for others (b) its role as a structural antagonist for vitamin B6 in those enzymes that it does not activate, and (c) the role of these analogues as competitive substrates for vitamin B6 in reactions leading to destruction of the vitamin.