Which of the following is NOT true regarding the MOA of prostaglandins for IOP control?

Prostaglandins, particularly those used in the treatment of elevated intraocular pressure (IOP), primarily work by enhancing the outflow of aqueous humor through the uveoscleral pathway. The correct answer highlights that the function of prostaglandins does not involve targeting alpha-2 (α2) receptors on macular cells (MACI).

In ocular pharmacology, prostaglandins like latanoprost and bimatoprost act mainly by binding to PGF2α receptors located on the ciliary muscle. This interaction leads to a process that modifies the extracellular matrix via the action of matrix metalloproteinases (MMPs), which subsequently reduces the collagen in the proximity of the uveoscleral outflow pathway and enhances the drainage of aqueous humor.

Regarding the other statements, they are accurate representations of the known mechanisms of action of prostaglandins. They indeed facilitate increased uveoscleral outflow, and MMPs play a role in remodeling the tissue to support this enhanced drainage. Therefore, it's essential to understand that concerning the pharmacological properties of prostaglandins, the targeting of α2 receptors is not part of their mechanism in lowering IOP.