For pristine SWCNTs KD = 62 ± 7 nM was obtained. SWCNTs of low defect density showed 9 KD = 21 ± 9 nM and SWCNTs of high defect density KD = 35 ± 30 nM. The marginally lower KD found in G d -SWCNTs can be attributed to the more rigid DNA-corona, offering less conformational freedom in response to dopamine DNA/SWCNT interactions. RB is an organic dye and therefore expected to quench SWCNT fluorescence . Indeed, already low concentrations of RB strongly quenched the fluorescence of SWCNTs (Figure ). Quenching correlated with defect density and G d -SWCNTs were quenched less than pristine SWCNTs. Upon addition of dopamine, pristine SWCNTs quenched by RB increased their fluorescence by up to 3100 % (Figure ). In contrast to sensitivity, sensor selectivity was not affected by g-defects. Indeed, the fluorescence responses of G d -SWCNTs to the homologues epinephrine, norepinephrine and the interfering substance ascorbic acid were not affected by defect density (Figure ). In accordance with the slightly decreased dopamine response in G d -SWCNTs, the less flexible corona makes SWCNTs also more robust against RB induced fluorescence quenching (Figure ). The strong influence of only small amounts of RB emphasizes the importance of careful sample purification in the surfactant-free g-defect synthesis protocol. On the other hand, RB-quenched SWCNTS provide an interesting platform for the design of SWCNT based turn-on sensors. The extreme fluorescence increase observed here is most likely a displacement of RB by dopamine from the hydrophobic SWCNT surface. Hereby, the SWCNT is turned from a nearly dark (RB-quenched) state into a bright (dopamine induced) state. For in vivo applications of sensors the light should be able to reach also deeper tissue levels .