LNP023 hydrochloride is an orally bioavailable, highly potent and highly selective factor B inhibitor. LNP023 shows direct, reversible, and high-affinity binding to human factor B with a K D of 7.9 nM. LNP023 inhibits factor B with an IC 50 value of 10 nM In Vitro LNP023 demonstrates potent inhibition of alternative complement pathway (AP)-induced membrane attack complex (MAC) formation in 50% human serum (IC 50 value of 130 nM). ?\nLNP023 exhibits excellent selectivity over other proteases affording IC 50 values of >30 μM across a panel of 41 human proteases, including the AP protein factor D (>100 μM). MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo LNP023 (20-180 mg/kg; oral administration) prevents KRN (150 μL)-induced arthritis in mice and is effective upon prophylactic and therapeutic dosing in an experimental model of membranous nephropathy in rats. ?\nLNP023 exhibits moderate half-lives (T 1/2 ; Wistar Han rats 3.4 h, beagle dogs 5.5 h) and C max (Wistar Han rats 410 nM, beagle dogs 2200 nM) following oral administration (rat 30 and, dog 10 mg/kg). ?\nLNP023 exhibits terminal elimination half-lives (T 1/2 ; Wistar Han rats 7 h, beagle dogs 5.6 h) due to high plasma clearance (8, and 2 mL/min/kg respectively combined with large volumes of distribution (2.3, and 0.6 L/kg respectively) following intravenous administration (rat 1.0 and, dog 0.1 mg/kg). MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: C57BL/6 mice with KRN-induced arthritisDosage: 20, 60, and 180 mg/kg Administration: Orally gavaged; twice a day (b.i.d.) for 14 days Result: Blocked KRN-induced arthritis. Form:Solid IC50& Target:KD: 7.9 nM (factor B),IC50: 10 nM (factor B)