The pharmacological properties of a series of polymethylene α-ωbistrimethylammonium iodides with 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, and 18 carbon atoms in the polymethylene chain have been studied. The decane derivative (C10) causes neuromuscular block in the cat in doses of 30 μg./kg. intravenously, and is the most active member of the series in this respect. During such block, the excitability of nerve and muscle is retained, the effects of acetylcholine injected arterially are paralysed, and acetylcholine release by motor nerve terminals is not prevented. Tetanization of the motor nerve or injection of acetylcholine or potassium neither diminishes nor deepens the block. A phase of potentiation of the muscle twitch, fasciculations of the muscle, and repetitive responses to single nerve volleys precedes the block. During a partial block, tetanization of the muscle leads to a well-sustained contraction. In the cat, profound neuromuscular block of the tibialis muscle may be caused by C10, without paralysis of respiratory muscles. With d-tubocurarine chloride respiratory paralysis accompanies or may precede paralysis of tibialis. C10 is 50–100 times less active by mouth than by intravenous injection. Its activity in cats anaesthetized with chloralose or pentothal is similar to that in the unanaesthetized cat; but ether appears to antagonize it slightly. Sensitivity to C10 varies greatly with species: in order of decreasing sensitivity, the series is cat-man - rabbit - monkey - mouse - rat. For d-tubocurarine chloride by the same tests, the variation in sensitivity is much smaller and decreases: rat-mouse-rabbit-cat. The action of C10 is not antagonized by anticholinesterases. The pentane and hexane homologues (C5, C6) are effective antagonists; the antagonism appears to be by competitive inhibition. Previous administration of d-tubocurarine chloride also reduces the effectiveness of C10. C10 and its neighbours elicit a contracture of the frog's rectus abdominis muscle, and do not antagonize the contracture elicited by acetylcholine. C5 and C6 do not elicit such a contracture, but antagonize the actions both of C10 and of acetylcholine. C10 can also elicit a twitch of cat's tibialis muscle if a small dose is given by close arterial injection. Members of the series, particularly C5 and C6, are able to block ganglionic transmission. Higher members possess a weak anticholinesterase action, which is more active against “true” cholinesterase than against “pseudo” cholinesterase. They also possess a weak muscarine-like action, a weak power of releasing histamine, and a feeble antibacterial action. No significant atropine-like action, or ability to stimulate autonomic ganglia, was detected. With the exception of C18, members of the series display negligible activity in depressing the surface tension of water. The pharmacological properties of the series have been related to the length of the polymethylene chain. This reveals four features: (1) a sharp maximum for potency in ganglionic block at C5–C6; (2) a sharp maximum for potency in neuromuscular block at C10; (3) a less well-defined maximum for muscarine-like activity, stimulation of frog's rectus, and anticholinesterase activity about C12; (4) a rise in antibacterial activity and surface activity beginning about C12 and still increasing at C18. The significance of the species difference, of the competitive antagonism of C5 for C10, of the variation of activity with length of polymethylene chain, and of the differences between C10 and d-tubocurarine chloride is discussed. It is a pleasure to express our indebtedness to Dr. Harold King for his interest and guidance throughout this investigation, and to our colleagues for many fruitful discussions and criticisms. We are also indebted to Dr. T. S. Work for advice on determining anticholinesterase activity, to Miss Bashford for assistance in these determinations, and to Dr. J. Niven for the histological examinations.