HBcAg (core antigen) is a hepatitis B viral protein. It is an indicator of active viral replication; this means the person infected with Hepatitis B can likely transmit the virus on to another person.
Calpastatin (184-210), an acetylated synthetic peptide derived from human calpastatin, effectively inhibits the calcium-dependent cysteine proteases, calpain I (µ-calpain) and calpain II (m-calpain), which require micromolar and millimolar calcium concentrations, respectively. Unlike its action on calpains, this 27 amino acid peptide does not inhibit papain (a cysteine protease) or trypsin (a serine protease). Encoded by exon 1B of Ac-calpastatin (184-210), it aligns with a section of inhibitory domain 1, showcasing its specificity and inhibitory function towards calpain enzymes.
SB-277011 dihydrochloride is a potent, selective, orally bioavailable and brain penetrate antagonist of dopamine D3 receptor(pKis of 8.0, 6.0, <5.2 and 5.9 for D3, D2, 5-HT1B, and 5-HT1D receptors, respectively).
Rineterkib hydrochloride (compound B) is an orally active RAF and ERK1 2 inhibitor in the treatment of a proliferative disease characterized by activating mutations in the MAPK pathway. The activity is particularly related to the treatment of KRAS-mutant NSCLC, BRAF-mutant NSCLC, KRAS-mutant pancreatic cancer, KRAS-mutant colorectal cancer (CRC) and KRAS-mutant ovarian cancer[1]. ERK-IN-1 (compound B) (50, 75 mg kg, p.o., qd q2d, 27 days) treatment significantly reduces the tumor volume in the Calu-6 human NSCLC subcutaneous tumor xenograft model in mice[1]. [1]. CAPONIGRO, et al. THERAPEUTIC COMBINATIONS COMPRISING A RAF INHIBITOR AND A ERK INHIBITOR. WO2018051306A1.
β-Endorphin (1-27) is an endogenous peptide that binds to μ-, δ-, and κ-opioid receptors (Kis = 5.31, 6.17, and 39.82 nM, respectively, in COS-1 cells expressing rat receptors). It binds to rat and mouse brain membrane preparations (IC50s = 1.1 and 5.7 nM, respectively) and induces chemotaxis of human monocytes in vitro when used at a concentration of 1 nM. Intracerebroventricular administration of β-endorphin (1-27) increases the latency to tail withdrawal in response to thermal stimulation in mice with a median antinociceptive dose (AD50) of 1,500 pmol per animal. It inhibits antinociception induced by β-endorphin in mice in response to thermal stimuli when administered at a dose of 65 pmol per animal. In rats, β-endorphin (1-27) does not affect drug-associated place preference when administered at doses up to 20 μg, i.c.v., but inhibits β-endorphin-induced place preference when administered at a dose of 10 μg per animal.