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Abstract Prolonged ultraviolet exposure results in the formation of cyclobutane pyrimidine dimers (CPDs) in RNA. Consequently, prebiotic photolesion repair mechanisms should have played an important role in the maintenance of the structural integrity of primitive nucleic acids. 2,6‐Diaminopurine is a prebiotic nucleobase that repairs CPDs with high efficiency when incorporated into polymers. We investigate the electronic deactivation pathways of 2,6‐diaminopurine‐2′‐deoxyribose and 9‐methyl‐2,6‐diaminopurine in acetonitrile and aqueous solution to shed light on the photophysical and excited state properties of the 2,6‐diaminopurine chromophore. Evidence is presented that both are photostable compounds exhibiting similar deactivation mechanisms upon the population of the S₁(ππ* L_a) state at 290 nm. The mechanism involves deactivation through the C2‐ and C6‐reaction coordinates and >99% of the excited state population decays through nonradiative pathways involving two conical intersections with the ground state. The radiative and nonradiative lifetimes are longer in aqueous solution compared to acetonitrile. Whileτ₁is similar in both derivatives,τ₂is ca. 1.5‐fold longer in 2,6‐diaminopurine‐2′‐deoxyribose due to a more efficient trapping in the S₁(ππ* L_a) minimum. Therefore, 2,6‐diaminopurine could have accumulated in significant quantities during prebiotic times to be incorporated into non‐canonical RNA and play a significant role in its photoprotection.