DC-98-LC74

DC-98-LC74 (0.01-100 μM) enhances the activity of adult muscle-type acetylcholine receptor (α1β1δε) in HEK293 cells, with an EC₅₀ value of 6.5 μM^[1].
DC-98-LC74 (10 μM; 10 min pre-incubation) significantly increases the maximal activation level of adult human muscle AChR in response to ACh in CN21-CHRNG knockout cells, without altering the EC₅₀ of ACh^[1].
DC₅₀-98-LC74 (0.001-100 μM) exhibits higher selectivity for human adult muscular AChR over human neuronal AChR subtypes (α7, α3β4, α4β2) in HEK293 cells. It shows only extremely weak PAM activity against α7 and α4β2, inhibitory activity against α3β4, and no agonist activity^[1].
DC₅₀-98-LC74 (30 μM) significantly prolongs the maximum burst duration of human adult wild-type muscular AChR in transfected HEK293 cells, increasing the average tau value from 5.02 ms to 30.0 ms^[1].
DC-98-LC74 (30 μM) significantly prolongs the maximum burst duration of εP141Leu and βIle308Ser FCMS mutant muscular AChRs in transfected HEK293 cells, restoring the burst duration to the level of WT adult AChRs^[1].
DC-98-LC74 (30 μM) causes no significant change in the burst duration of human fetal wild-type muscular AChR in transfected HEK293 cells^[1].
DC-98-LC74 (1-100 μM) dose-dependently increases the channel open probability of human adult wild-type muscle AChR (EC₅₀ = 7.8 μM) and εP141Leu FCMS mutant AChR (EC₅₀ = 78.9 μM) in transfected HEK293 cells, with approximately 10-fold lower potency toward the mutant receptor^[1].
DC-98-LC74 (30 μM) increases the cluster open probability and prolongs the channel open time of human adult wild-type muscle AChR in transfected HEK293 cells^[1].
The activity of DC₅₀-98-LC74 (30 μM) in prolonging the burst duration of adult human muscle AChR in transfected HEK293 cells requires the juxtamembrane M2-M3 loop of the ε subunit, whereas replacing this region with the corresponding region of the fetal γ subunit abolishes its activity^[1].
DC-98-LC74 (30 µM) prolongs the decay time constant of miniature endplate currents (mEPC) from 1.19 ms to 2.15 ms in mouse phrenic nerve/hemidiaphragm preparations^[1].
DC-98-LC74 (1-30 µM) reverses fatigue-related reduction in twitch amplitude and increases twitch amplitude and area under the curve in a dose-dependent manner in isolated extensor digitorum longus (EDL) neuromuscular preparations from aged sarcopenic mice^[1].

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