Corilagin

The best-characterized action. Corilagin restrains the NLRP3 inflammasome via ROS/TXNIP and blocks pyroptosis ^{4Reference 4Luo J et al. · 2022Corilagin restrains NLRP3 inflammasome activation and pyroptosis through the ROS/TXNIP axisView study →}, inhibits NLRP3 through Olfr2 signaling to alleviate atherosclerosis ^{11Reference 11Mao J et al. · 2024Corilagin alleviates atherosclerosis by inhibiting NLRP3 inflammasome activation via the Olfr2 pathwayView study →}, and reduces acute lung injury by inhibiting RIP1-driven necroptosis (with SPR-confirmed target binding) ^{12Reference 12Ye J et al. · 2025Corilagin alleviates acute lung injury by inhibiting RIP1-driven necroptosisView study →} — with genus-level NF-κB/MAPK support from Terminalia tannin fractions ^{15Reference 15Ekambaram SP et al. · 2022The hydrolysable-tannin fraction of Terminalia chebula modulates NF-κB and MAPK signallingView study →}.

Gap: each study uses a different disease model and a different upstream node, with no single dose/target replicated head-to-head, and the TNF-α/NF-κB effects are downstream readouts rather than proven primary targets ^{4,12Reference 4Luo J et al. · 2022Corilagin restrains NLRP3 inflammasome activation and pyroptosis through the ROS/TXNIP axisView study →Reference 12Ye J et al. · 2025Corilagin alleviates acute lung injury by inhibiting RIP1-driven necroptosisView study →}.

The real isolate antiviral story is herpesvirus. Corilagin protected against HSV-1 encephalitis via TLR2 inhibition ^{8Reference 8Guo YJ et al. · 2015Corilagin protects against HSV-1 encephalitis via inhibiting the TLR2 signalling pathwaysView study →}, interfered with TLR3-mediated responses in herpes-simplex encephalitis ^{9Reference 9Li LJ et al. · 2019Corilagin interferes with the TLR3-mediated immune response in herpes-simplex encephalitisView study →}, and blocked HSV-2 replication via the cGAS–STING axis ^{10Reference 10Zhang H et al. · 2026Corilagin interferes with HSV-2 replication via the cGAS–STING axisView study →}.

Gap: the “anti-HBV / Phyllanthus” reputation is not supported by isolated-corilagin data — that traces to whole-decoction work — so the isolate signal is herpesvirus, not hepatitis B ^{8Reference 8Guo YJ et al. · 2015Corilagin protects against HSV-1 encephalitis via inhibiting the TLR2 signalling pathwaysView study →}.

Corilagin inhibited ovarian cancer growth by blocking TGF-β/Smad/ERK/AKT ^{5Reference 5Jia L et al. · 2013Corilagin inhibits ovarian cancer growth by blocking the TGF-β signalling pathwayView study →} and suppressed esophageal squamous-cell carcinoma via DNA damage and RNF8 downregulation with cisplatin sensitization ^{6Reference 6Qiu F et al. · 2019Corilagin in esophageal squamous-cell carcinoma: DNA damage and RNF8 downregulationView study →}, as synthesized in a dedicated review ^{13Reference 13Gupta A et al. · 2019Corilagin in cancer: a critical evaluation of anticancer activities and molecular mechanismsView study →}.

Gap: cell-line and xenograft only, at high in-vitro concentrations, with no pharmacokinetic bridge to achievable human exposure — nowhere near clinical ^{5,6Reference 5Jia L et al. · 2013Corilagin inhibits ovarian cancer growth by blocking the TGF-β signalling pathwayView study →Reference 6Qiu F et al. · 2019Corilagin in esophageal squamous-cell carcinoma: DNA damage and RNF8 downregulationView study →}.

Corilagin restored glutathione and SOD, lowered ALT/AST, and suppressed TNF-α/NF-κB/COX-2 in a bioassay-guided Phyllanthus niruri study ^{1Reference 1Ezzat SM et al. · 2020In-depth hepatoprotective mechanistic study of Phyllanthus niruri: in-vitro and in-vivo studies and its chemical characterizationView study →} — where it also contributes α-glucosidase inhibition in the extract assays ^{2Reference 2Najari Beidokhti M et al. · 2017Investigation of antidiabetic potential of Phyllanthus niruri (α-glucosidase)View study →}.

Gap: corilagin is one of several actives in the fraction, so the effect is co-attributed, not cleanly isolate-only ^{1Reference 1Ezzat SM et al. · 2020In-depth hepatoprotective mechanistic study of Phyllanthus niruri: in-vitro and in-vivo studies and its chemical characterizationView study →}.

Corilagin potentiates β-lactams against MRSA by inactivating the resistance protein PBP2a ^{3Reference 3Shiota S et al. · 2004Mechanisms of action of corilagin and tellimagrandin I that remarkably potentiate the activity of beta-lactams against methicillin-resistant Staphylococcus aureusView study →}.

Gap: in-vitro only, and narrow — an adjuvant effect rather than a standalone antibiotic, with no in-vivo confirmation ^{3Reference 3Shiota S et al. · 2004Mechanisms of action of corilagin and tellimagrandin I that remarkably potentiate the activity of beta-lactams against methicillin-resistant Staphylococcus aureusView study →}.