Table 4.

CARM1-specific inhibitors.

Structure and numbering	Activity		year[ref]
	Biochemical	Cellular
	Assay: RGA IC50 around 8 μM (CARM1 with PABP1 as substrate); Certain inhibition on PRMT3, -5 and -6, but weaker than on CARM1; Inactive to tested HKMTs (SET7/9, G9a, DOT1L, Suv39H1).	Compound 21 suppressed the methylation of the transfected PABP1 protein in HEK293 cells; From androgen-driven luciferase assay, both compounds showed dose-dependent inhibition of the transcription level was observed starting from 4 μM.	2011[72]
	Assay: RFA Both: IC50 0.06 μM for (CARM1); Inactive to PRMT1 and SET7/9 (IC50 > 100 μ)	Compound 34: No inhibition was observed for cellular methylation of H3R26 at 5 μM for 48 h; No significant activity in the hormone-M) dependent assays (IC50 > 10 μM).	2009[81]
		Biochemical
		Assay: RFA IC50 (CARM1): Compound 23, 1.8 μM; Compound 24–27, 0.08–0.23 μM; Compound 26: inactive to PRMT1 and -3 (IC50 > 25 μM); moderate permeability against PAMPA.	2008[82], 2009[83]
		Assay: RFA IC50 (CARM1): compound 28–32, 0.04–0.06 μM; Compound 31: inactive to PRMT1 and -3 (IC50 > 25 μM); improved permeability.	2009[83]
		Assay: RFA IC50 = 0.2 – 0.9 μM; Better pharmacokinetics profile (lower clearance, longer half-life and smaller volumes of distribution) compared with compound 33.	2009[84]
		Assay: RFA Compound 41: IC50 0.07 μM (CARM1); Inactive to PRMT1 and -3 (IC50 > 25 μM); Compound 42: IC50 0.12μM (CARM1);	2009[85]
		Assay: RFA IC50 around 0.03 μM (CARM1); Inactive to PRMT1 and -3 (IC50 > 25 μM); Crystal structures available	2011[86]
		Assay: SPA IC50 0.80 μM for SETD2, 2.2 μM for SET7/9, 3.0 μM for CARM1, 9.5 μM for PRMT1, >100 μM for SET8, G9a, and GLP.	2015[98]