LN5972 

LN5972 is a selective ACKR3 agonist with an EC₅₀ of 3.40 μM, showing higher selectivity for ACKR3 over CXCR4. LN5972 induces β-arrestin recruitment to ACKR3/CXCR7. LN5972 reduces the surface expression of P-selectin. LN5972 is applicable to studies related to platelet-mediated thrombosis^[1].

1. This compound can be used as a tracer.
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.

LN5972 (0.3 nM-100 μM) acts as a superagonist for ACKR3 in HEK293T cells, inducing β-arrestin recruitment with an EC₅₀ of 3.40 μM and a maximal efficacy 161% that of CXCL12^[1].
LN5972 (100 μM; 15 min preincubation) reduces CRP-XL-induced P-selectin expression by 76% in human platelet-rich plasma^[1].
LN5972 (0.3 nM-100 μM) is selective for ACKR3 and shows no activity at CXCR4 in HEK293T cells^[1].
LN5972 shows high metabolic stability in human liver microsomes (87% remaining at 120 min) and reduced stability in mouse liver microsomes^[1].
LN5972 (up to 100 μM; 72 h) is non-cytotoxic to THP1 and HEK293 cells^[1].

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

422.54

C₁₉H₃₀N₆O₃S

3035425-93-2

O=C(N1CCN(CCCNC2=NN3C(C=C(CC)N=C3S2)=O)CC1)OC(C)(C)C

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Bayrak A, et al. Discovery and Development of First-in-Class ACKR3/CXCR7 Superagonists for Platelet Degranulation Modulation. J Med Chem. 2022;65(19):13365-13384.  [Content Brief]