Step 1: Recall the pharmacological strategies aimed at diabetic retinopathy. They target the biochemical pathways of hyperglycaemic damage, including the polyol pathway, advanced glycation end products, protein kinase C activation and oxidative stress.
Step 2: Place each correct option in its pathway. Benfotiamine, a lipid-soluble thiamine derivative, blocks several hyperglycaemia-driven pathways and reduces advanced glycation end products. Ruboxistaurin is a selective protein kinase C beta inhibitor studied to slow visual loss in diabetic retinopathy. Pyridazinones have been investigated as agents that improve retinal microvascular function.
Step 3: Examine the odd one out. Tamoxifen is a selective oestrogen receptor modulator used in breast cancer. It has no role in diabetic retinopathy and is in fact itself a recognised cause of drug-induced retinopathy with crystalline deposits.
Step 4: Conclude. The drug NOT used for diabetic retinopathy is tamoxifen.