AbstractNarrow concentration intervals were used, covering 10−6– 10−4Mdesaspidin. The interaction with glycolysis involves three steps, the inhibitor constants (Ki:s) being in turn 2.7 × 10−5M, 1.3 × 10−4M, and high. About 18% of total glycolysis is inhibited in each of the two first steps, and 65% left for the third reaction. After compensation for glycolysis, oxidative phosphorylation may show a sudden jump to about 10% inhibition at 1.5 × 10−5Mdesaspidin, the possibleKiof the reaction starting here being very high. Correcting for glycolysis, desaspidin affects total Photophosphorylation in two steps, with theKivalues of 7.8 × 10−5Mand 4.6 × 10−4Mrespectively. Inhibition in the first step is about 27% of the total photophosphorylation.By applying 10−6MDCMU[/3‐(3, 4‐dichlorophenyl)‐l, l‐dimethy lurea], one can abolish non‐cyclic photophosphorylation. Desaspidin then reacts in a single step with aKiof 1.4 × 10−4M. At 5 × 10−5MDCMU, also the pseudocyclic photophosphorylation is abolished. The remaining, true cyclic photophosphorylation has a singleKiof 2.3 × 10−5Mfor desaspidin.Under non‐cyclic conditions, the true cyclic process contributes about 25% to total Photophosphorylation. Under pseudocyclic conditions, no cyclic photophosphorylation occurs. Under true cyclic conditions, the non‐cyclic and pseudocyclic processes are inoperative. This indicates a regulative system, so that either (1) the (non‐cyclic + true cyclic), (2) only the pseudocyclic, or (3) only the true cyclic systems can be traced, dependent on the level of DCMU applied. There are two sites for non‐cyclic Photophosphorylation, one of them common to the pseudocyclic pathway. Cyclic photophosphorylati