Propoxycaine for COVID-19
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COVID-19 Treatment Clinical Evidence
COVID-19 involves the interplay of 400+ viral and host proteins and factors, providing many therapeutic targets.
c19early analyzes 6,000+ studies for 210+ treatments—over 17 million hours of research.
Only three high-profit early treatments are approved in the US.
In reality, many treatments reduce risk,
with 25 low-cost treatments approved across 163 countries.
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Naso/
oropharyngeal treatment Effective Treatment directly to the primary source of initial infection. -
Healthy lifestyles Protective Exercise, sunlight, a healthy diet, and good sleep all reduce risk.
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Immune support Effective Vitamins A, C, D, and zinc show reduced risk, as with other viruses.
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Thermotherapy Effective Methods for increasing internal body temperature, enhancing immune system function.
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Systemic agents Effective Many systemic agents reduce risk, and may be required when infection progresses.
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High-profit systemic agents Conditional Effective, but with greater access and cost barriers.
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Monoclonal antibodies Limited Utility Effective but rarely used—high cost, variant dependence, IV/SC admin.
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Acetaminophen Harmful Increased risk of severe outcomes and mortality.
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Remdesivir Harmful Increased mortality with longer followup. Increased kidney and liver injury, cardiac disorders.
Propoxycaine may be beneficial for
COVID-19 according to the study below.
COVID-19 involves the interplay of 400+ viral and host proteins and factors providing many therapeutic targets.
Scientists have proposed 11,000+ potential treatments.
c19early.org analyzes
210+ treatments.
We have not reviewed propoxycaine in detail.
, Broad-spectrum inhibition of SARS-CoV-2 variants by dibutyl phthalate through allosteric disruption of Spike-ACE2 interface, Frontiers in Microbiology, doi:10.3389/fmicb.2025.1610775
Introduction The persistent evolution of SARS-CoV-2 has diminished the efficacy of existing vaccines and antibodies, increasing the risks of reinfection and Long COVID. There is a significant need for the development of convenient, broad-spectrum antiviral agents that target the early stage of viral infection. Traditional Chinese Medicine (TCM) volatile oils, with their diverse components and suitability for nasal delivery, demonstrate potential against respiratory viruses. This study aimed to screen bioactive compounds from TCM volatile oils for their ability to inhibit the interaction between the SARS-CoV-2 spike (S) protein and its host receptor, ACE2. Methods A virtual screening of 47 structurally diverse TCM volatile compounds was performed to identify potential inhibitors of the Spike-ACE2 interaction. The top candidate, dibutyl phthalate (DBP), was further evaluated using in vitro assays including Spike-mediated membrane fusion and pseudovirus infection. Its mechanism was investigated through ELISA, surface plasmon resonance (SPR), ACE2 enzymatic activity assays, molecular docking. To evaluate its broad-spectrum potential, membrane fusion assays were further performed using spike proteins from the wild-type (WT), Delta, and Omicron XBB.1.5 variants. Critical binding residues were identified through molecular docking and subsequently confirmed by site-directed mutagenesis of the Spike receptor-binding domain (RBD). Results Virtual screening identified ten potential inhibitors, with dibutyl phthalate (DBP) showing the strongest activity. DBP effectively inhibited S protein-mediated membrane fusion ( IC 50 = 64.53 μM) and pseudovirus infection ( IC 50 = 73.06 μM) with specificity. SPR analysis confirmed that DBP competitively inhibited the binding between the S trimer and ACE2 (increasing the K D from 8.28 nM to 86.7 nM). Mechanistic studies revealed that DBP disrupts the S-ACE2 interaction by targeting the receptor-binding domain (RBD) without affecting ACE2 enzymatic activity. Furthermore, DBP exhibited broad-spectrum inhibitory activity against membrane fusion mediated by the Delta ( IC 50 = 49.22 μM) and Omicron XBB.1.5 ( IC 50 = 53.70 μM) spike variants. Molecular docking and subsequent site-directed mutagenesis identified Tyr453 and Tyr495 as critical residues for DBP binding and its inhibitory function. ..