Table 2 Therapeutic strategies associated with cell death of SARS-CoV-2

From: The role of cell death in SARS-CoV-2 infection

Drug	Host target	Type of cell death	Mechanism
Infliximab	TNF-α	Apoptosis	Acts as a chimeric IgG1 monoclonal antibody that targets TNF-α.^64,65
Emricasan	Pan-caspase	Apoptosis	Suppresses caspase-3/7/9.^66,67
Q-VD	Pan-caspase	Apoptosis	Suppresses caspase-3.⁶⁸
Primidone	RIPK1	Necroptosis	Reduces RIPK1-mediated necroptosis.⁸³
Necrostatin-1	RIPK1	Necroptosis	Acts as a RIPK1-targeted inhibitor of necroptosis.^84,85
MCC950	NLRP3	Pyroptosis	Inhibits SARS-CoV-2 N-induced cytokine production.⁹⁷
Dapansutrile	NLRP3	Pyroptosis	Inhibits the production of early cytokines.¹⁰⁴
Disulfiram	GSDMD	Pyroptosis	Modifies Cys191/Cys192 in GSDMD to block pore formation, which prevents IL-1β release.¹⁰⁵
Disulfiram	GSDMD	NETosis	Downregulation of innate immune and complement/coagulation pathways to reduce NET formation.^163,164
Telmisartan	Angiotensin receptors	Pyroptosis	Inhibits Ang binding with its receptors, which leads to a reduction in the Ang-ATR signaling.¹⁰⁶
Anakinra	IL-1 receptor	Pyroptosis	Blocks NLRP3 inflammasome-dependent pyroptosis.¹⁰⁷
Canakinumab	IL-1β	Pyroptosis	A human monoclonal antibody that targets IL-1β.¹⁰⁸
Tocilizumab	IL-6 receptor	Pyroptosis	An IL-6 receptor antagonist.¹¹⁰
Tocilizumab	Iron ion	Ferroptosis	Iron chelation.¹²⁹
Imatinib	Free iron	Ferroptosis	Binds with free iron to inactivate iron-containing enzymes and inhibits Fenton reactions.¹²⁷
Selenium	GPX4	Ferroptosis	Preserves GPX4 from irreversible inactivation due to its role in selenocysteine synthesis.^{130,131,132,133}
Ebselen	GPX4	Ferroptosis	Prevents ferroptosis by acting as a GPX mimic.¹³²
Ebselen	M of SARS-CoV-2	Ferroptosis	Inhibits viral replication by interacting with SARS-CoV-2 M protein.¹³¹
N-acetylcysteine	GSH	Ferroptosis	Reinforces the GPX4-GSH-cysteine axis.^136,137
Ferrostatin-1	Free iron	Ferroptosis	Captures free radicals and slows down the accumulation of PLOOH in PUFA.^138,139
Liproxstatin-1	Free iron	Ferroptosis	Captures free radicals and slows down the accumulation of PLOOH in PUFA.^138,139
Sivelestat	NE	NETosis	A selective NE inhibitor.¹⁵⁸
Cl-amidine	PAD4	NETosis	Reduces histone citrullination in both SARS-CoV-2-infected neutrophils.¹⁴⁹
Apremilast	PDE4	NETosis	A PDE4 selective inhibitor.¹⁶¹
DNase-I	NETs	NETosis	Dissolves thrombogenic NETs.¹⁶²
Dipyridamole	PDE	NETosis	A PDE inhibitor.¹⁷¹
Alvelestat	NE	NETosis	Inhibits neutrophil elastase.¹⁷³

TNF-α tumor necrosis factor-alpha, IgG1 immunoglobin G1, RIPK1 receptor interacting serine/threonine kinase 1, NLRP3 PYD domain-containing protein 3, GSDMD gasdermin-D, NET neutrophil extracellular traps, Ang II angiotensin II, ATR serine/threonine kinase, IL‑1 interleukin 1, IL-6 interleukin 6, GPX4 glutathione peroxidase, GSH glutathione, ACSL4 acyl-CoA synthetase long-chain family member 4, PLOOH phospholipid hydroperoxides, PUFA polyunsaturated fatty acids, NE neutrophil elastase, PAD4 protein arginine deiminase 4, PDE4 phosphodiesterase 4, NET extracellular traps

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Table 2 Therapeutic strategies associated with cell death of SARS-CoV-2

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