Abstract
Conspectus SARS-CoV-2 is the etiological pathogen of the COVID-19 pandemic, which led to more than 6.5 million deaths since the beginning of the outbreak in December 2019. The unprecedented disruption of social life and public health caused by COVID-19 calls for fast-track development of diagnostic kits, vaccines, and antiviral drugs. Small molecule antivirals are essential complements of vaccines and can be used for the treatment of SARS-CoV-2 infections. Currently, there are three FDA-approved antiviral drugs, remdesivir, molnupiravir, and paxlovid. Given the moderate clinical efficacy of remdesivir and molnupiravir, the drug-drug interaction of paxlovid, and the emergence of SARS-CoV-2 variants with potential drug-resistant mutations, there is a pressing need for additional antivirals to combat current and future coronavirus outbreaks. In this Account, we describe our efforts in developing covalent and noncovalent main protease (Mpro) inhibitors and the identification of nirmatrelvir-resistant mutants. We initially discovered GC376, calpain inhibitors II and XII, and boceprevir as dual inhibitors of Mpro and host cathepsin L from a screening of a protease inhibitor library. Given the controversy of targeting cathepsin L, we subsequently shifted the focus to designing Mpro-specific inhibitors. Specifically, guided by the X-ray crystal structures of these initial hits, we designed noncovalent Mpro inhibitors such as Jun8-76-3R that are highly selective toward Mpro over host cathepsin L. Using the same scaffold, we also designed covalent Mpro inhibitors with novel cysteine reactive warheads containing di- and trihaloacetamides, which similarly had high target specificity. In parallel to our drug discovery efforts, we developed the cell-based FlipGFP Mpro assay to characterize the cellular target engagement of our rationally designed Mpro inhibitors. The FlipGFP assay was also applied to validate the structurally disparate Mpro inhibitors reported in the literature. Lastly, we introduce recent progress in identifying naturally occurring Mpro mutants that are resistant to nirmatrelvir from genome mining of the nsp5 sequences deposited in the GISAID database. Collectively, the covalent and noncovalent Mpro inhibitors and the nirmatrelvir-resistant hot spot residues from our studies provide insightful guidance for future work aimed at developing orally bioavailable Mpro inhibitors that do not have overlapping resistance profile with nirmatrelvir.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 157-168 |
| Number of pages | 12 |
| Journal | Accounts of chemical research |
| Volume | 56 |
| Issue number | 2 |
| DOIs | |
| State | Published - Jan 17 2023 |
| Externally published | Yes |
ASJC Scopus subject areas
- Chemistry(all)
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Tan, B., Joyce, R., Tan, H., Hu, Y. (2023). SARS-CoV-2 Main Protease Drug Design, Assay Development, and Drug Resistance Studies. Accounts of chemical research, 56(2), 157-168. https://doi.org/10.1021/acs.accounts.2c00735
SARS-CoV-2 Main Protease Drug Design, Assay Development, and Drug Resistance Studies. / Tan, Bin; Joyce, Ryan; Tan, Haozhou et al.
In: Accounts of chemical research, Vol. 56, No. 2, 17.01.2023, p. 157-168.
Research output: Contribution to journal › Article › peer-review
Tan, B, Joyce, R, Tan, H, Hu, Y 2023, 'SARS-CoV-2 Main Protease Drug Design, Assay Development, and Drug Resistance Studies', Accounts of chemical research, vol. 56, no. 2, pp. 157-168. https://doi.org/10.1021/acs.accounts.2c00735
Tan B, Joyce R, Tan H, Hu Y, Wang J. SARS-CoV-2 Main Protease Drug Design, Assay Development, and Drug Resistance Studies. Accounts of chemical research. 2023 Jan 17;56(2):157-168. doi: https://doi.org/10.1021/acs.accounts.2c00735
Tan, Bin ; Joyce, Ryan ; Tan, Haozhou et al. / SARS-CoV-2 Main Protease Drug Design, Assay Development, and Drug Resistance Studies. In: Accounts of chemical research. 2023 ; Vol. 56, No. 2. pp. 157-168.
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abstract = "Conspectus SARS-CoV-2 is the etiological pathogen of the COVID-19 pandemic, which led to more than 6.5 million deaths since the beginning of the outbreak in December 2019. The unprecedented disruption of social life and public health caused by COVID-19 calls for fast-track development of diagnostic kits, vaccines, and antiviral drugs. Small molecule antivirals are essential complements of vaccines and can be used for the treatment of SARS-CoV-2 infections. Currently, there are three FDA-approved antiviral drugs, remdesivir, molnupiravir, and paxlovid. Given the moderate clinical efficacy of remdesivir and molnupiravir, the drug-drug interaction of paxlovid, and the emergence of SARS-CoV-2 variants with potential drug-resistant mutations, there is a pressing need for additional antivirals to combat current and future coronavirus outbreaks. In this Account, we describe our efforts in developing covalent and noncovalent main protease (Mpro) inhibitors and the identification of nirmatrelvir-resistant mutants. We initially discovered GC376, calpain inhibitors II and XII, and boceprevir as dual inhibitors of Mpro and host cathepsin L from a screening of a protease inhibitor library. Given the controversy of targeting cathepsin L, we subsequently shifted the focus to designing Mpro-specific inhibitors. Specifically, guided by the X-ray crystal structures of these initial hits, we designed noncovalent Mpro inhibitors such as Jun8-76-3R that are highly selective toward Mpro over host cathepsin L. Using the same scaffold, we also designed covalent Mpro inhibitors with novel cysteine reactive warheads containing di- and trihaloacetamides, which similarly had high target specificity. In parallel to our drug discovery efforts, we developed the cell-based FlipGFP Mpro assay to characterize the cellular target engagement of our rationally designed Mpro inhibitors. The FlipGFP assay was also applied to validate the structurally disparate Mpro inhibitors reported in the literature. Lastly, we introduce recent progress in identifying naturally occurring Mpro mutants that are resistant to nirmatrelvir from genome mining of the nsp5 sequences deposited in the GISAID database. Collectively, the covalent and noncovalent Mpro inhibitors and the nirmatrelvir-resistant hot spot residues from our studies provide insightful guidance for future work aimed at developing orally bioavailable Mpro inhibitors that do not have overlapping resistance profile with nirmatrelvir.",
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N2 - Conspectus SARS-CoV-2 is the etiological pathogen of the COVID-19 pandemic, which led to more than 6.5 million deaths since the beginning of the outbreak in December 2019. The unprecedented disruption of social life and public health caused by COVID-19 calls for fast-track development of diagnostic kits, vaccines, and antiviral drugs. Small molecule antivirals are essential complements of vaccines and can be used for the treatment of SARS-CoV-2 infections. Currently, there are three FDA-approved antiviral drugs, remdesivir, molnupiravir, and paxlovid. Given the moderate clinical efficacy of remdesivir and molnupiravir, the drug-drug interaction of paxlovid, and the emergence of SARS-CoV-2 variants with potential drug-resistant mutations, there is a pressing need for additional antivirals to combat current and future coronavirus outbreaks. In this Account, we describe our efforts in developing covalent and noncovalent main protease (Mpro) inhibitors and the identification of nirmatrelvir-resistant mutants. We initially discovered GC376, calpain inhibitors II and XII, and boceprevir as dual inhibitors of Mpro and host cathepsin L from a screening of a protease inhibitor library. Given the controversy of targeting cathepsin L, we subsequently shifted the focus to designing Mpro-specific inhibitors. Specifically, guided by the X-ray crystal structures of these initial hits, we designed noncovalent Mpro inhibitors such as Jun8-76-3R that are highly selective toward Mpro over host cathepsin L. Using the same scaffold, we also designed covalent Mpro inhibitors with novel cysteine reactive warheads containing di- and trihaloacetamides, which similarly had high target specificity. In parallel to our drug discovery efforts, we developed the cell-based FlipGFP Mpro assay to characterize the cellular target engagement of our rationally designed Mpro inhibitors. The FlipGFP assay was also applied to validate the structurally disparate Mpro inhibitors reported in the literature. Lastly, we introduce recent progress in identifying naturally occurring Mpro mutants that are resistant to nirmatrelvir from genome mining of the nsp5 sequences deposited in the GISAID database. Collectively, the covalent and noncovalent Mpro inhibitors and the nirmatrelvir-resistant hot spot residues from our studies provide insightful guidance for future work aimed at developing orally bioavailable Mpro inhibitors that do not have overlapping resistance profile with nirmatrelvir.
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FAQs
What is the main protease of SARS-CoV-2 mutations? ›
SARS-CoV-2 Mpro is a homodimeric cysteine protease, which processes the majority of the viral polyproteins pp1a and pp1ab encoded by the ORF1a/b gene.
How does the SARS-CoV-2 protease work? ›SARS-CoV-2 produces a spike protein that binds to host cell receptor ACE2 for entry. (1,2) Upon entry, the positive genomic RNA of SARS-CoV-2 will attach directly to the host ribosome and translate two large polyproteins, which are then processed by proteolysis into components for packaging new virions.
What are natural inhibitors for SARS-CoV-2? ›Ferulic acid and its derivatives, including caffeoyltyramine, feruloyltyramine, and feruloyloctopamine, also inhibit SARS-CoV PLpro activity (Li, 2015).
What proteins are needed for SARS-CoV-2 infection? ›In addition to these genes, SARS-CoV-2 contains genes that encode four structural proteins which are involved in infectious virus assembly: (S)pike, (E)nvelope), (M)embrane, and (N)ucleocapsid) proteins.
What is the most important protein for SARS-CoV-2? ›Spike glycoprotein
The envelope of corona-virion contains protruding projection from its surface called spike proteins (or S proteins). The Spike glycoprotein mediates the virus attachment to host cell surface receptors ACE2 and facilitates virus entry by assisting fusion between viral and host cell membranes.
Q: What does a positive SARS-CoV-2 antibody test result mean? A: A positive antibody test result could mean you previously had a SARS-CoV-2 infection or COVID-19. A positive antibody test could also mean the test is detecting antibodies in your blood in response to your COVID-19 vaccine.
How does SARS-CoV-2 suppress the immune system? ›SARS-CoV-2 may also meddle with MHC-I, a protein that displays bits of the invader on the surface of infected cells and summons T cells. Viral proteins such as ORF6 and ORF8 may curb cells' production of MHC-I or block its transfer to the cell surface, preventing T cells from recognizing and killing infected cells.
What are the side effects of protease enzymes? ›Proteolytic enzymes are generally considered safe but can cause side effects in some people. It's possible you may experience digestive issues like diarrhea, nausea and vomiting, especially if you take very high doses (34).
What herbs for SARS-CoV-2? ›Roughly, 25.000 herb-based preparations and extracts have been employed in traditional medicine in South Asia. In recent times, a decoction of maricha (Piper nigrum), lavanga (Syzygium aromaticum), and sunthi (Zingiber officinaleRoscoe.) have been suggested for both healthy and COVID-19 patients.
What drugs are effective against SARS-CoV-2? ›Recently several drugs have been used as anti-SARS-CoV-2 such as Remdesivir, Favipiravir, Hydroxychloroquine, Azithromycin, Lopinavir/Ritonavir, Nafamostat mesylate and so on.
What are the new drugs for SARS-CoV-2? ›
As noted above, Veklury (remdesivir) is approved for the treatment of COVID-19 in adults and pediatric patients (28 days of age and older and weighing at least 3 kilograms) with positive results of direct SARS-CoV-2 viral testing, who are: hospitalized, or not hospitalized and have mild-to-moderate COVID-19 and are at ...
What does SARS-CoV-2 spike protein mean? ›One of the key biological characteristics of SARS-CoV-2, as well as several other viruses, is the presence of spike proteins that allow these viruses to penetrate host cells and cause infection.
What does anti SARS-CoV-2 spike protein positive mean? ›Your Spike Protein Antibody results will be reported as a reference range: >/= 0.80 U/mL: This is a positive result for anti-SARS CoV-2S. A positive result means your body's immune system has generated a response to the COVID-19 vaccine.
Which type of viral test detects proteins of SARS-CoV-2? ›Nucleic Acid Amplification Testing for SARS-CoV-2 Infection. Reverse transcription polymerase chain reaction (RT-PCR)-based diagnostic tests (which detect viral nucleic acids) are considered the gold standard for detecting current SARS-CoV-2 infection.
What do SARS-CoV-2 nucleocapsid antibody test results mean? ›If you have a positive test result (antibodies are detected), you may have been infected with the virus that causes COVID-19 at some point in the past. There is still a chance that the antibodies indicate past infection due to other coronaviruses.
What is considered positive for SARS-CoV-2 IgG antibodies? ›The antibody test is performed with a patient's blood specimen and will detect antibodies to SARS-CoV2. If the blood sample tests positive for the antibody, this likely indicates that the person was previously infected with the virus that causes COVID-19.
What is the antibody response after SARS-CoV-2 infection and implications for immunity? ›Data synthesis: Moderate-strength evidence suggests that most adults develop detectable levels of IgM and IgG antibodies after infection with SARS-CoV-2 and that IgG levels peak approximately 25 days after symptom onset and may remain detectable for at least 120 days.
Is SARS-CoV-2 infection a trigger of autoimmune response? ›We observed that patients having a de novo autoimmune response had the worst acute viral disease prognosis and outcome. Our results sustain the hypothesis that COVID-19 infection correlates with the autoimmunity markers.
What does SARS-CoV-2 affect mainly? ›Extrapulmonary Manifestations
Although COVID-19, the illness caused by SARS-CoV-2, predominantly affects the respiratory system, COVID-19 can be considered a systemic viral illness given the multiple organ dysfunction associated with this illness.
Combined, these data indicate that SARS-CoV-2 infection leads to widespread degradation of host mRNAs both by the activation of RNase L, and by a second RNase L-independent mechanism.
What symptoms might a person have if they did not make protease enzyme? ›
When the pancreas doesn't naturally secrete digestive enzymes, it affects your body's ability to break down the foods you eat and absorb nutrients. This can lead to malnutrition as well symptoms such as bloating, cramping, gassiness, and diarrhea.
What diseases are caused by protease? ›Protease activity has been implicated in the pathogenesis of vascular diseases including atherosclerosis, thrombosis, and aneurysm. A wide variety of proteases representing different proteolytic families and their corresponding inhibitors are involved.
What are the symptoms of protease deficiency? ›Protease deficiency is associated with dryness. Dry extremities and dry skin rashes are usually the rule. Constipation, calcium deficiency, gingivitis, fungus, hypertension, hearing loss, tooth decay and mood swings are symptoms associated with protease deficiency.
What is the drug of choice for SARS cov2 causing COVID-19 infection? ›Full FDA approval: Remdesivir is indicated for treatment of COVID-19 in adults and pediatric patients aged 12 years and older (weighing at least 40 kg) who require hospitalization, or those are not hospitalized and have mild-to-moderate COVID-19 and are at high risk for progression to severe COVID-19, including ...
What are the best antiviral herbs for coronavirus? ›Some of the antiviral medicinal plant species are citrus Spp., orange (C. Sinensis), Allium sativum, Allium cepa, Mentha piperita, and nigella sativa are the most desirable herbal drink or fruit that can introduce effective adjuvant components in COVID-19 management.
What home remedies can I use to treat Covid? ›- Keep a daily routine, such as taking a shower and getting dressed.
- Take breaks from COVID-19 news and social media.
- Eat healthy meals and drink plenty of fluids.
- Stay physically active.
- Get plenty of sleep.
- Avoid use of drugs, tobacco and alcohol.
Remdesivir is the only antiviral drug that is approved by the Food and Drug Administration (FDA) for the treatment of COVID-19.
What medication prevents COVID from getting worse? ›Remdesivir tends to work best in the beginning stages of COVID-19 infection when the virus is working hard to replicate itself in your body. Ideally, outpatient remdesivir treatment should start within seven days of infection.
How is SARS-CoV treated? ›Remdesivir has shown in vitro activity against SARS-CoV-2 in combination with chloroquine (Wang M. et al., 2020) or in monotherapy, as part of a 10-day intravenous treatment in COVID-19 patients with severe pneumonia (Adaptive COVID-19 Treatment Trial ACTT-NCT04280705) (Beigel et al., 2020).
Which FDA approved drugs reduced SARS-CoV-2 infection in lab? ›Panobinostat had the strongest effect on limiting SARS-CoV-2 replication whilst maintaining cell viability, and completely blocked replication of SARS-CoV-2 at all doses tested (Figure 5); however, if cells were infected prior to treatment a more modest effect on replication were observed.
Is there any alternative receptor for SARS-CoV-2? ›
CD147, known as basigin or extracellular matrix metalloproteinase inducer (EMMPRIN), acts as an alternative receptor for SARS-CoV-2 entry into cells with low or undetectable ACE2 expression [30,39].
What is the anti viral effect of remdesivir against SARS-CoV-2? ›Remdesivir was shown to exhibit antiviral activity against SARS-CoV-2 in vitro studies, and it was proposed as an investigational drug early during the pandemic.
What are SARS-CoV-2 recombinant variants? ›Recombination: A process in which the genomes of two SARS-CoV-2 variants combine during the viral replication process to form a new variant that is different from both parent lineages. This may occur when a person is infected with two variants at the same time.
Which SARS-CoV-2 mutations are responsible for immune evasion leading to breakthrough infection? ›Our study adds to the growing body of evidence linking rapidly emerging mutations in the S and ORF genes of the SARS-CoV-2 genome to immune evasion. It is clear that in addition to B. 1.617, B. 1 and A strains can also evade vaccine-induced immune responses, even after two rounds of vaccination.
What does SARS-CoV-2 virus contain? ›The genome of the new coronavirus shows similarities to other β-CoV found in bats. SARS-CoV-2 is 96.2% identical to a bat CoV RaTG13, whereas it shares 79.5% identity to SARS-CoV.
What are the 4 types of nucleotides found in SARS-CoV-2? ›Although many nucleotides exist in nature, only 4 nucleotides, labeled A, C, G, and T, have been found in DNA. They are abbreviations of Adenine, Cytosine, Guanine, and Thymine. Although it is difficult to put viruses in the category of living organisms, they also have genetic codes made up of nucleotides.
What variant is SARS-CoV-2 assay? ›The FDA's Analysis:This test is now expected to detect the SARS-CoV-2 omicron variant (B. 1.1.
What are other names for SARS-CoV-2 mRNA vaccine? ›The FDA has also approved the Moderna vaccine, now called Spikevax, to prevent COVID-19 in people age 18 and older. The FDA has given emergency use authorization to Moderna COVID-19 vaccines for age 6 months to age 17.
Is SARS-CoV-2 same as Omicron? ›Currently, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread worldwide as an Omicron variant. This variant is a heavily mutated virus and designated as a variant of concern by the World Health Organization (WHO).
Does SARS-CoV-2 affect the immune system? ›Taken together, the investigators write, these findings suggest that SARS-CoV-2 infection damages the CD8+ T cell response, an effect akin to that observed in earlier studies showing long-term damage to the immune system after infection with viruses such as hepatitis C or HIV.
Is SARS-CoV-2 the same as Corona? ›
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus first identified in Wuhan, China, in December 2019. It became a pandemic throughout 2020 and into 2021. Infection with SARS-CoV-2 leads to a potentially severe respiratory illness called COVID-19.
How is SARS-CoV-2 COVID diagnosed? ›Viral tests, including Nucleic Acid Amplification Tests (NAATs, such as PCR tests), antigen tests and other tests (such as breath tests) are used as diagnostic tests to detect current infection with SARS-CoV-2, determine the need for prevention measures like isolation, and to inform an individual's medical care.
How different is SARS-CoV-2 from other coronaviruses? ›Cowl says that SARS-CoV-2 is likely more contagious than the viruses that cause influenza and common cold because it is new to humans. Humans have no way to prepare for it, and their immune systems are not ready to fight it. This results in the virus causing more cellular damage and producing more inflammatory cells.
What type of cells are most affected by SARS-CoV-2? ›Primary cultured epithelia are readily infected with SARS-CoV-2 and release a substantial amount of virus from the apical cell surface. 6 8 9 In the nasal epithelium, both ciliated and mucus-secreting goblet cells express ACE2 and TMPRSS2.
What are the major antigens of the SARS-CoV-2 virus? ›The SARS-CoV-2 antigens on this array include spike protein (S), the receptor-binding (RBD), S1, and S2 domains the whole protein (S1+S2), and the nucleocapsid protein (NP). There is a similar set of antigens represented on the array from SARS-CoV, MERS-CoV, and the four common cold coronaviruses.
Is SARS-CoV-2 RNA or PCR? ›The Quest Diagnostics SARS-CoV-2 RNA, Qualitative Real-Time RT-PCR (“Quest SARS-CoV-2 rRT-PCR”) is a real-time RT-PCR test intended for the qualitative detection of nucleic acids from SARS-CoV-2 in upper and lower respiratory specimens (such as nasopharyngeal or oropharyngeal swabs, sputum, tracheal aspirates, and ...