Etripamil (MSP-2017) displays atrioventricular nodal conduction and prolongs atrioventricular nodal refractory periods by inhibiting calcium ion influx through the calcium slow channels in the atrioventricular node cells. Etripamil is an antagonist of short-acting L-type calcium-channel. It has a rapid onset of action designed for intranasal administration. It is also used to treat Paroxysmal Supraventricular Tachycardia.

Ravulizumab (ALXN1210) is a humanized monoclonal antibody targeting complement factor 5 that specifically binds to human complement protein C5 with high affinity to block complement activation. Ravulizumab can be used for the prevention and treatment of paroxysmal sleep hemoglobinuria, atypical hemolytic uremic syndrome and myasthenia gravis.

Crovalimab (SKY59; RO7112689) is a novel humanized antibody designed to target C5 in a pH-dependent manner, demonstrating binding affinities (KD) of 15.2 nM and 16.8 μM at pH levels of 7.4 and 5.8, respectively. Additionally, it shows high affinity for human FcRn at pH 6.0, with a KD of 17 μM. By blocking C5 cleavage by C5 convertase and inhibiting the activity of a C5 variant (p.Arg885His), Crovalimab effectively prevents the formation of C5b-9 across the classical (CP), lectin (LP), and alternative (AP) complement pathways. This characteristic highlights its potential utility in research concerning paroxysmal nocturnal hemoglobinuria (PNH) and other complement-mediated diseases.

Iptacopan hydrochloride (LNP023 hydrochloride) is an orally bioavailable, highly potent and highly selective factor B inhibitor with an IC50 of 10 nM. Iptacopan hydrochloride shows direct, reversible, and high-affinity binding to human factor B with a KD of 7.9 nM.

Complement component C3 plays a particularly versatile role in this process by keeping the cascade alert, acting as a point of convergence of activation pathways, fueling the amplification of the complement response, exerting direct effector functions, and helping to coordinate downstream immune responses[3]. In C3-/- mice alcohol-induced liver steatosis is absent or strongly reduced after chronic or acute alcohol exposure. This suggests that the complement system and its component C3 contribute to the development of alcohol-induced fatty liver and its consequences[4].AMY-101 TFA (Cp40 TFA) is a peptidic inhibitor of the central complement component C3 (KD: 0.5 nM). It shows a favorable anti-inflammatory activity in models with COVID-19 severe pneumonia with systemic hyper inflammation[5].a daily subcutaneous dose of AMY-101 (4 mg/kg bodyweight) was protective against NHP periodontitis, suggesting that patients treated for systemic disorders (e.g., paroxysmal nocturnal hemoglobinuria) can additionally benefit in terms of improved periodontal condition[6].Plasma concentrations of both C3 and Cp40 were measured periodically and complete saturation of plasma C3 was confirmed. No differences in hematological, biochemical, or immunological parameters were identified in the blood or tissues of animals treated with Cp40 when compared to those injected with vehicle alone. Further, skin wounds showed no signs of infection in those treated with Cp40.Cp40 treatment was associated with a trend toward accelerated wound healing when compared with the control group. In addition, a biodistribution study in a rhesus monkey indicated that the distribution of Cp40 in the body is associated with the presence of C3, concentrating in organs that accumulate blood and produce C3[7].

Danicopan (ACH-4471) (ACH-4471) is a selective, orally active small molecule factor D inhibitor with high binding affinity to human factor D, with a Kd value of 0.54 nM. Danicopan (ACH-4471) inhibits the activity of the complement replacement pathway (APC) and may block the complement replacement pathway in paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS).

Flecainide acetate is a class Ic antiarrhythmic agent, it is used to treat a variety of cardiac arrhythmias including paroxysmal atrial fibrillation, paroxysmal supraventricular tachycardia, and ventricular tachycardia. It works by regulating the flow of

DPPY is a potent inhibitor of PTK that acts on EGFR (IC50<10 nM), BTK (IC50<10 nM), and JAK3 (IC50<10 nM). DPPY inhibits the proliferation of B-cell lymphoma cells and has potential for investigation in idiopathic pulmonary fibrosis (IPF).