DLK-IN-2 

DLK-IN-2 is a selective inhibitor of DLK and neuroprotective agent. DLK-IN-2 shows no significant inhibition against CYPs 3A4, 2D6 and 2C9. DLK-IN-2 inhibits acute axonal palmitoylation of DLK, blocks DLK-dependent pro-degenerative axon-to-soma retrograde signaling and suppresses c-Jun phosphorylation. DLK-IN-2 can be used for the mechanistic study of neurodegenerative diseases^[1].

DLK-IN-2 (compound 13) (10 μM; 1 h pre-incubation, 2.5 h post-deprivation) significantly inhibits trophic factor deprivation-induced c-Jun phosphorylation in primary embryonic day 16 rat DRG neurons^[1].
DLK-IN-2 (10 μM; 1 h pre-incubation, 45 h post-deprivation) significantly protects primary embryonic day 16 rat DRG neurons from trophic factor deprivation-induced neurodegeneration^[1].
DLK-IN-2 (10 μM; 4 h post-injury) transiently reduces acute axotomy-induced Wallerian degeneration in primary embryonic day 16 rat DRG neuron spot cultures, but does not protect axons at 6 h post-injury^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

444.97

C₂₃H₂₅ClN₂O₃S

883012-32-6

O=S(C1=CC=C(NC(C2=CC=C(Cl)C=C2)=O)C=C1)(NC34CC5CC(C4)CC(C5)C3)=O

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• [1]. Zhang X, et al. Combinatorial chemistry identifies additional compounds that selectively inhibit DLK-dependent retrograde signaling while minimally affecting other axonal roles of DLK. Sci Rep. 2026;16(1):3892. Published 2026 Jan 27.  [Content Brief]