LY2112688

LY2112688 (Ac-(d-Arg)-CEH-(d-Phe)-RWC-NH2) (1 pM-10 μM) exhibits K_i values of 165, 74, 0.13, and 1713 nM for human MC1R, MC3R, MC4R, and MC5R, respectively, in competitive binding assays using membranes from recombinant BHK570 cells expressing these receptors, demonstrating high binding affinity and selectivity for human MC4R^[2].
LY2112688 (100 nM-10 μM; 3 h; ±10 μM Propranolol (HY-B0573B)) promotes NEFA release from human subcutaneous white adipose tissue explants; Propranolol does not significantly reduce LY2112688-induced NEFA release, but shows a decreasing trend^[2].
LY2112688 does not promote GLP-1 release from mouse colonic crypt preparations^[4].
LY2112688 promotes GLP-1 release from mouse distal small intestine perfusion preparations^[4].
LY2112688 produces a concentration-dependent antisecretory response in wild-type mouse distal colonic mucosa when administered basolaterally, with an EC₅₀ of 23.9 nM^[4].
The antisecretory response of LY2112688 in the colonic mucosa of C57BL/6J mice is Y1 receptor-dependent and is antagonized by the MC4R antagonist HS014, supporting the involvement of MC4R-PYY-Y1 signaling in this effect^[4].
LY2112688 inhibits fecal pellet transport in isolated C57BL/6J mouse colon, manifesting as slowed colonic motility^[4].
LY2112688 (100 nM) induces a maximal MC4R-cAMP response in N2A_HA-MC4R-GFP cells, comparable to that of α-MSH and MTII used to produce maximal responses^[6].
LY2112688 (100 nM; washed out after approximately 10 min; restimulated with 500 nM α-MSH (HY-P0252)) induces cAMP signaling in N2A_HA-MC4R-GFP cells that rapidly disappears after removal of LY2112688, and upon restimulation with α-MSH, the cAMP response recovers to a level comparable to that of the initial stimulation^[6].
LY2112688 (100 nM) induces MC4R internalization in N2A_HA-MC4R-GFP cells, with a receptor internalization rate comparable to that of other MC4R agonists in that study^[6].
LY2112688 (500 nM; 4 h) promotes intracellular accumulation of MC4R in N2A_HA-MC4R-GFP cells, with the extent of intracellular retention comparable to the level induced by α-MSH^[6].
LY2112688 (500 nM; 4 h; re-stimulation with the same agonist for 15 min) induces MC4R desensitization in N2A_HA-MC4R-GFP cells, reducing the intracellular cAMP response upon re-agonist stimulation by approximately 40% compared with acute stimulation^[6].
LY2112688 (1 pM-10 μM) exhibits IC₅₀ values of 820, 27, 0.10, and 1239 nM in competitive binding assays for mouse MC1R, MC3R, MC4R, and MC5R, respectively, demonstrating high binding affinity and selectivity for mouse MC4R^[7].
LY2112688 (1 pM-10 μM; 30 min) does not elevate cAMP levels in differentiated 3T3-L1 adipocytes^[7].
LY2112688 (300 nM; 1-15 min) promotes ERK1/2 phosphorylation in differentiated 3T3-L1 adipocytes, with the strongest effect at 5 min, followed by a decrease thereafter; under these conditions, LY2112688 does not increase PKB phosphorylation^[7].
LY2112688 (0.1 nM-10 μM) concentration-dependently promotes ERK1/2 phosphorylation in differentiated 3T3-L1 adipocytes and reaches a relatively high level at approximately 1 μM^[7].
Treatment with LY2112688 does not increase AMPK or JNK phosphorylation levels in undifferentiated 3T3-L1 adipocytes^[7].
LY2112688 (100 nM-10 μM; 3 h) promotes lipolysis in human subcutaneous white adipose tissue explants derived from non-obese women, increasing NEFA release by 46% over vehicle at 100 nM and promoting glycerol release, with a maximal lipolytic response lower than that of isoproterenol^[2].
LY2112688 (1 pM-10 μM; 2 h) does not promote NEFA release from human subcutaneous differentiated adipocytes derived from obese men, and the same negative result is obtained in human visceral adipocytes^[2].
LY2112688 (1 pM-10 μM; 3 h) promotes NEFA release from differentiated 3T3-L1 adipocytes with an EC₅₀ of 5270 nM, and the E_max is below 400 μM NEFA, with no clear plateau E_max obtained due to its weak effect^[7].
LY2112688 (1 pM-10 nM; 3 h) does not promote NEFA release from primary adipocytes isolated from mouse epididymal adipose tissue^[7].

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