It's interesting that famotidine is being studied (in combination with hydroxychloroquine in this case) based on observations in China that patients on famotidine had better outcomes:
https://www.msn.com/...-19/ar-BB13fflX
What's really interesting to me is that famotidine's possible action against SARS-CoV-2 was previously and independently predicted through docking studies:
https://www.scienced...211383520302999
This gives me some hope that other docking studies might also find compounds that work. Here's what I've been taking for the past few weeks. Most or all have been discussed here already, but it doesn't hurt to re-post in this new light of possible independent confirmation of one of them (3 docking studies cited below and 2 others). Comments mine:
For prophylaxis and initial infection: Viral replication is greatest in the first week when there are less serious symptoms. Final outcomes (death or recovery) seem to depend somewhat or largely on the viral load in this first stage, so it's essential to stop replication as much as possible as soon as possible!:
Vitamin D (2500IU per day or higher). Daily doses are prefered over higher weekly doses for various reasons.
Vitamin D status is significantly associated with clinical outcomes. A multinomial logistic regression analysis reported that for each standard deviation increase in serum 25(OH)D, the odds of having a mild clinical outcome rather than a severe outcome were approximately 7.94 times (OR=0.126, p<0.001) while interestingly, the odds of having a mild clinical outcome rather than a critical outcome were approximately 19.61 times (OR=0.051, p<0.001). The results suggest that an increase in serum 25(OH)D level in the body could either improve clinical outcomes or mitigate worst (severe to critical) outcomes, while a decrease in serum 25(OH)D level in the body could worsen clinical outcomes of COVID-2019 patients.
Quercetin (dosing of 500mg 2x/d for prophylaxis or 500mg or more 4x/d if there's an active infection) seems promising for several reasons. It was found in this study to have high affinity to the spike protein of covid-19. It's also a zinc ionophore (like hydroxychloroquine with out the side effects). This is also the subject of clinical studies.
Luteolin is also noted to have even slightly higher binding affinity:
Zinc supplementation is indicated too and may work with quercetin to inhibit viral replication, 40mg/d for prophylaxis, 80mg/d for active infection.
From the ranking, 47 ligands were found to form S- protein:ACE2 interface-ligand binding complexes with scores equal to or better than the score threshold (Vina score better and -7 kcal/mol)
This docking study found that Sylibinin (from milk thistle) and also quercetin (among others) could be effective against covid-19 by targeting its main protease.
Of the compounds found in this study to be likely of benefit against covid-19, the ones most broadly indicated that is also available as a supplement are hesperidin, neohesperidin, and Andrographiside (from andrographis). This study also found Famotidine (Pepcid) to possibly be useful.
This is probably most useful during an infection and especially in the 2nd week. The second week is when people usually progress to serious disease if it's going to happen. At this point there's less viral replication (so that ship may have sailed, if you didn't prevent it earlier), and now it's time to damp down immune overreaction, etc.:
Melatonin 40mg to 80mg (in divided doses) is being used with some success to treat covid-19. This study indicated that it might work. Melatonin also downregulates bradykinin which could reduce the capillary leakage which has recently been suggested to be responsible for some of the morbidity and perhaps fatalities. It is currently being used with reported success in several places:
Melatonin was reported in potential antiviral infection via its anti-inflammatory and antioxidant effects
58,59,60,61,62. Melatonin indirectly regulates ACE2 expression, a key entry receptor involved in viral infection of HCoVs, including 2019-nCoV/SARS-CoV-2 (ref.
33). Specifically, melatonin was reported to inhibit calmodulin and calmodulin interacts with ACE2 by inhibiting shedding of its ectodomain, a key infectious process of SARS-CoV
72,73. JUN, also known as c-Jun, is a key host protein involving in HCoV infectious bronchitis virus
74. As shown in Fig.
6d, mercaptopurine and melatonin may synergistically block c-Jun signaling by targeting multiple cellular targets. In summary, combination of mercaptopurine and melatonin may offer a potential combination therapy for 2019-nCoV/SARS-CoV-2 by synergistically targeting papain-like protease, ACE2, c-Jun signaling, and anti-inflammatory pathways (Fig.
6d).
Edited by smithx, 28 April 2020 - 06:17 AM.
This topic is locked
) It is very confusing trying to make sense of the available literature.
