Реестр препаратов-кандидатов для лечения и профилактики COVID-19
TAK-981 is a selective inhibitor of the SUMOylation enzymatic cascade, with potential immune-activating and anti-tumor activities.
Aviptadil is a synthetic version of Vasoactive Intestinal Polypeptide (VIP). This protein is found throughout the body and contributes to numerous functions including vasodilation, increasing glycogenolysis, lowering arterial blood pressure, and relaxing the smooth muscles. VIP is highly concentrated in the lung, where it prevents NMDA-induced caspase-3 activation in the lung, inhibits IL6, and TNFa production. It is theorized that the delivery of this therapeutic will help with the serious lung complications associated with COVID-19.
Azvudine (RO-0622) is an antiviral drug which acts as a reverse transcriptase inhibitor. It was developed for the treatment of Hepatitis C.
Macrolides may have immunomodulatory properties in pulmonary inflammatory disorders. They may downregulate inflammatory responses and reduce the excessive cytokine production associated with respiratory viral infections; however, their direct effects on viral clearance are uncertain. Immunomodulatory mechanisms may include reducing chemotaxis of neutrophils (PMNs) to the lungs by inhibiting cytokines (i.e., IL-8), inhibition of mucus hypersecretion, decreased production of reactive oxygen species, accelerating neutrophil apoptosis, and blocking the activation of nuclear transcription factors.
Азоксимера бромид обладает комплексным действием: иммуномодулирующим, детоксицирующим, антиоксидантным, противовоспалительным. Увеличивает резистентность организма в отношении локальных и генерализованных инфекций бактериальной, грибковой и вирусной этиологии.
Основным механизмом иммуномодулирующего действия азоксимера бромида является прямое воздействие на фагоцитирующие клетки и естественные киллеры, а также стимуляция антителообразования, синтеза интерферона-альфа и интерферона-гамма.
Acalabrutinib is approved to creat a pair of blood cancers: chronic lymphocytic leukemia and mantle cell lymphoma. It is used to treat a type of non-Hodgkin lymphoma known as mantle cell lymphoma.
Аллоферон представляет собой олигопептид. По характеру фармакологического действия наиболее сходен с интерфероном альфа. Аллоферон является эффективным индуктором синтеза эндогенных интерферонов и активатором системы естественных киллеров, способен стимулировать распознавание и лизис дефектных клеток цитотоксическими лимфоцитами.
Хронический рецидивирующий герпес 1 и 2 типов, в составе комплексной терапии в среднетяжелой (желтушной) формы острого гепатита В.
Acetylcysteine protects against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione. It does this by producing the glutathione precursor L-cysteine. Glutathione is required to inactivate an intermediate metabolite (N-acetyl-p-benzoquinoneimine or NAPQI) of acetaminophen that is thought to be hepatotoxic. In acetaminophen overdose cases, excessive quantities of this metabolite are formed because the primary metabolic (glucuronide and sulfate conjugation) pathways become saturated.
Acetylcysteine may act by reducing the metabolite to the parent compound and/or by providing sulfhydryl for conjugation of the metabolite. Experimental evidence also suggests that a sulfhydryl-containing compound such as acetylcysteine may also directly inactivate the metabolite. The mechanisms of action for acetylcysteine’s well-known mucolytic effects are different.
In particular, when inhaled, acetylcysteine (and its metabolic byproduct cysteine) exerts its mucolytic action through its free sulfhydryl group, which reduces the disulfide bonds in the mucus matrix and lowers mucus viscosity. This action increases with increasing pH and is most significant at pH 7 to 9. The mucolytic action of acetylcysteine is not affected by the presence of DNA. Acetylcysteine is also an antioxidant and reduces oxidative stress.
Acetylcysteine serves as a prodrug to L-cysteine which is a precursor to the biologic antioxidant, glutathione and hence administration of acetylcysteine replenishes glutathione stores. L-cysteine also serves as a precursor to cystine which in turn serves as a substrate for the cystine-glutamate antiporter on astrocytes hence increasing glutamate release into the extracellular space. This glutamate in turn acts on mGluR2/3 receptors, and at higher doses of acetylcysteine, mGluR5. Glutathione also modulates the NMDA receptor by acting at the redox site. These effects on glutamate and NMDA signaling appear to explain some of the positive neuropsychotropic effects associated with NAC.
Acetylcysteine also possesses some anti-inflammatory effects possibly via inhibiting NF-κB through redox activation of the nuclear factor kappa kinases thereby modulating cytokine synthesis.
Baloxavir marboxil is an influenza therapeutic agent, specifically, an enzyme inhibitor targeting the influenza virus' cap-dependent endonuclease activity, one of the activities of the virus polymerase complex. In particular, it inhibits a process known as cap snatching, by which the virus derives short, capped primers from host cell RNA transcripts, which it then uses for polymerase-catalyzed synthesis of its needed viral mRNAs. A polymerase subunit binds to the host pre-mRNAs at their 5′-caps, then the polymerase's endonuclease activity catalyzes its cleavage "after 10–13 nucleotides". As such, its mechanism is distinct from neuraminidase inhibitors such as oseltamivir and zanamivir.
Janus kinases are intracellular enzymes that transmit signals arising from cytokine or growth factor receptor interactions on the cellular membrane to influence cellular processes of immune cell function and hematopoiesis. JAK-mediated signaling is pivotal in immune activation, as cytokine receptors are expressed on most immune cells. Within the signaling pathway, JAKs phosphorylate and activate signal transducers and activators of transcription proteins (STATs), which modulate intracellular activity including gene expression. Baricitinib modulates the signaling pathway at the point of JAKs, preventing the phosphorylation and activation of STATs. Cytokine signaling is transmitted through pairing of JAKs. Baricitinib has greater affinity for JAK1, JAK2, and TYK2, relative to JAK3. In human leukocytes, baricitinib inhibits cytokine induced STAT phosphorylation mediated by JAK1/JAK2, JAK1/JAK3, JAK1/TYK2, or JAK2/TYK2 with comparable potencies