Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Dual-targeting cancer and SARS-CoV-2: The host-directed mechanisms of Spatholobus suberectus Dunn (Jixueteng).
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Ganesan Kumar, Chen Jianping
Аннотация
BACKGROUND: Spatholobus suberectus Dunn (SSD), known in traditional Chinese medicine as Jixueteng, has historically been used to treat conditions characterized by blood stasis. Modern research has validated its anticancer potential. Recent studies reveal broad-spectrum antiviral activity.
PURPOSE: This review synthesizes these two research frontiers. It proposes a unified host-directed therapy paradigm as the core mechanism underlying SSD's dual therapeutic capability.
METHODS: A comprehensive analysis of peer-reviewed literature was conducted. This included phytochemical studies, in vitro and in vivo pharmacological investigations, and computational modeling related to SSD. Emphasis was placed on integrating the latest mechanistic findings on its antiviral action against SARS-CoV-2 with its established anticancer profile.
RESULTS: SSD contains bioactive flavonoids, such as isoliquiritigenin and procyanidins. These compounds enable multi-target interactions with host proteins. In cancer, SSD acts as a host-directed anticancer agent by inhibiting lactate dehydrogenase A, activating AMP-activated protein kinase, inducing apoptosis and pyroptosis, and arresting the cell cycle at the G2/M checkpoint. Against SARS-CoV-2, SSD functions as a direct inhibitor of the host angiotensin-converting enzyme 2 receptor. It blocks viral entry with pan-variant efficacy validated in vivo. The anticancer evidence for SSD is extensive and derived from multiple independent laboratories. The antiviral data are currently more limited. Published studies have identified SSD as active against SARS-CoV-2 and demonstrated that isoliquiritigenin inhibits viral replication via NRF2 activation. Mechanistic ACE2-targeting data remain preliminary. A comparative synthesis reveals that SSD's efficacy in both oncology and virology converges on the modulation of host protein targets. SSD targets dysregulated host enzymes in cancer and a hijacked host receptor in viral infection. This strategy provides a high barrier to therapeutic resistance.
CONCLUSION: SSD represents a promising natural host-directed therapeutic platform. Its dual ability to disrupt cancer cell physiology and inhibit SARS-CoV-2 entry via distinct host targets positions it as a potential template for developing resistance-evasive strategies against complex diseases. Future efforts must focus on isolating the precise ACE2-inhibiting compounds, optimizing disease-specific delivery, and advancing translational studies to realize its clinical potential.
PURPOSE: This review synthesizes these two research frontiers. It proposes a unified host-directed therapy paradigm as the core mechanism underlying SSD's dual therapeutic capability.
METHODS: A comprehensive analysis of peer-reviewed literature was conducted. This included phytochemical studies, in vitro and in vivo pharmacological investigations, and computational modeling related to SSD. Emphasis was placed on integrating the latest mechanistic findings on its antiviral action against SARS-CoV-2 with its established anticancer profile.
RESULTS: SSD contains bioactive flavonoids, such as isoliquiritigenin and procyanidins. These compounds enable multi-target interactions with host proteins. In cancer, SSD acts as a host-directed anticancer agent by inhibiting lactate dehydrogenase A, activating AMP-activated protein kinase, inducing apoptosis and pyroptosis, and arresting the cell cycle at the G2/M checkpoint. Against SARS-CoV-2, SSD functions as a direct inhibitor of the host angiotensin-converting enzyme 2 receptor. It blocks viral entry with pan-variant efficacy validated in vivo. The anticancer evidence for SSD is extensive and derived from multiple independent laboratories. The antiviral data are currently more limited. Published studies have identified SSD as active against SARS-CoV-2 and demonstrated that isoliquiritigenin inhibits viral replication via NRF2 activation. Mechanistic ACE2-targeting data remain preliminary. A comparative synthesis reveals that SSD's efficacy in both oncology and virology converges on the modulation of host protein targets. SSD targets dysregulated host enzymes in cancer and a hijacked host receptor in viral infection. This strategy provides a high barrier to therapeutic resistance.
CONCLUSION: SSD represents a promising natural host-directed therapeutic platform. Its dual ability to disrupt cancer cell physiology and inhibit SARS-CoV-2 entry via distinct host targets positions it as a potential template for developing resistance-evasive strategies against complex diseases. Future efforts must focus on isolating the precise ACE2-inhibiting compounds, optimizing disease-specific delivery, and advancing translational studies to realize its clinical potential.