This paper discusses a modification of receptor theory, proposing that the relationship between drug concentration and tissue response is more complex than previously thought. Clark's original model assumed that the percentage of receptors occupied by a drug equals the percentage of the tissue's response. However, experiments with acetylcholine and other drugs showed that this assumption was not always valid. The paper suggests that the response of a tissue is not linearly proportional to the number of receptors occupied, and that different drugs may have varying capacities to initiate a response, a property known as efficacy. This means that a drug with high efficacy can produce a maximum response even when only a small proportion of receptors are occupied, while a drug with low efficacy may require a larger proportion of receptors to produce a response. The paper also discusses the effects of different alkyltrimethylammonium salts on guinea-pig ileum, showing that some of these compounds act as partial agonists, producing a response that is less than the maximum possible. The results suggest that the efficacy of these compounds varies, and that their effects are influenced by the number of receptors they occupy. The paper also discusses the effects of atropine on these compounds, showing that atropine can reduce the sensitivity of the tissue to the partial agonists. This suggests that the partial agonists occupy a significant proportion of the receptors when producing a response, unlike normal agonists. The paper concludes that the relationship between drug concentration and tissue response is more complex than previously thought, and that the concept of efficacy is essential for understanding this relationship. The results suggest that the affinity of drugs for receptors varies with chain length, and that the efficacy of drugs can be estimated from experimental data. The paper also discusses the implications of these findings for the understanding of drug antagonism, suggesting that the traditional model of competitive and non-competitive antagonism may need to be revised.This paper discusses a modification of receptor theory, proposing that the relationship between drug concentration and tissue response is more complex than previously thought. Clark's original model assumed that the percentage of receptors occupied by a drug equals the percentage of the tissue's response. However, experiments with acetylcholine and other drugs showed that this assumption was not always valid. The paper suggests that the response of a tissue is not linearly proportional to the number of receptors occupied, and that different drugs may have varying capacities to initiate a response, a property known as efficacy. This means that a drug with high efficacy can produce a maximum response even when only a small proportion of receptors are occupied, while a drug with low efficacy may require a larger proportion of receptors to produce a response. The paper also discusses the effects of different alkyltrimethylammonium salts on guinea-pig ileum, showing that some of these compounds act as partial agonists, producing a response that is less than the maximum possible. The results suggest that the efficacy of these compounds varies, and that their effects are influenced by the number of receptors they occupy. The paper also discusses the effects of atropine on these compounds, showing that atropine can reduce the sensitivity of the tissue to the partial agonists. This suggests that the partial agonists occupy a significant proportion of the receptors when producing a response, unlike normal agonists. The paper concludes that the relationship between drug concentration and tissue response is more complex than previously thought, and that the concept of efficacy is essential for understanding this relationship. The results suggest that the affinity of drugs for receptors varies with chain length, and that the efficacy of drugs can be estimated from experimental data. The paper also discusses the implications of these findings for the understanding of drug antagonism, suggesting that the traditional model of competitive and non-competitive antagonism may need to be revised.