Pharmacological mechanism and clinical application of ciprofol

Abstract

Propofol has become one of the most commonly used anesthetic agents because of its good sedative effects, rapid onset, and fast metabolism. However, its associated respiratory and circulatory depression and injection pain make it difficult for patients to tolerate. Ciprofol, which is structurally similar to propofol but has an additional cyclopropyl group, is less likely to impact respiratory and circulatory function and cause injection pain, highlighting its potential for clinical application. Currently, as research on Ciprofol is still in the exploratory stage, its clinical application is limited because its underlying mechanisms are not yet fully understood. The aim of this article is to review the pharmacological mechanisms of propofol, hypothesize the primary pharmacological effects and potential adverse reactions of Ciprofol, and summarize its current clinical application status, with the goal of providing a reference for future clinical use.

Keywords: GABA; anesthesia; ciprofol; propofol; sedation.

FIGURE 1

Schematic diagram of the chemical structure of propofol and ciprofol, with a schematic diagram of their binding to GABAA. The above is a schematic diagram of the chemical structure of propofol, and the following is a schematic diagram of the chemical structure of ciprofol, which binds more closely to the GABAA receptor and has a higher affinity.

FIGURE 2

Schematic diagram of the mechanism of the central sedative action of ciprofol production. The binding of ciprofol to the GABAA receptor results in a change in membrane potential, inhibiting glutamate release and ultimately producing a sedative effect. AMP: cyclic adenosine monophosphate, PKA: cyclic AMP-dependent protein kinase.

FIGURE 3

Schematic diagram of the mechanism by which ciprofol causes hypotension. Ciprofol promotes the release of nitric oxide (NO) by promoting protein kinase C (PKC) translocation, activating endothelial nitric oxide synthase (eNOS), thereby causing cyclic guanosine monophosphate (cGMP), which ultimately leads to vascular smooth muscle relaxation. O₂: oxygen, GC: guanylate cyclase, GTP: guanosine triphosphate, K⁺(Ca²⁺): calcium-activated potassium channels, K⁺ (ATP): ATP-sensitive potassium channels.