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PI(3,4,5)P3 lipid remodeling during pyroptotic cell death structurally stabilizes GSDMD pores at the plasma membrane.

CONCLUSIONS: Plasmodium infection is associated with canonical and non-canonical pyroptosis in splenic macrophages. R848 treatment was associated with reduced pyroptotic signaling in splenic macrophages, suggesting a regulatory role for TLR7.

For decades, scientists have understood that each of the roughly 20,000 genes in the human body carries instructions for a single kind of protein.

Pyrotech Therapeutics has dosed its first subject in Phase 1 study of PTT-121, the first selective GSDMD inhibitor, aiming to tackle septic shock and inflammatory diseases.

Clinical milestone validates the company's platform for drugging "undruggable" targets BEIJING, Sept. 1, 2026 /PRNewswire/ -- Pyrotech Therapeutics ("Pyrotech" or the "Company"), a clinical-stage biopharmaceutical company pioneering innate immune modulation and pyroptosis-targeted...

a–e, Activation of multiple regulated mLCD pathways in MC38 cells after aMPC16-CA50 (160 µg ml−1) treatment for varying durations. a, Immunoblotting of p-RIPK1, RIPK1, p-RIPK3, RIPK3, p-MLKL, or MLKL. The combined treatment of TNF, cycloheximide (CHX), and Z-VAD-FMK serves as the positive control. b, Immunoblotting of GSDME-N and GSDMD-N. TNF plus CHX and doxorubicin treatment serves as the positive control for GSDME-N and GSDMD-N induction, respectively. c,d, Lipid peroxidation evaluated by C11-BODIPY 581/591 staining. RSL3 treatment serves as positive control. c, Representative flow cytometry plots of C11-BODIPY 581/591 in MC38 cells. d, Relative lipid ROS is expressed as the ratio of oxidized to reduced C11-BODIPY MFI. e, Immunoblotting of cleaved PARP1 or caspase-3. Doxorubicin treatment serves as positive control. f–h, Viability of MC38 cells after treatment with aMPC16-CA50 (160 µg ml−1) for 24 h in the absence or presence of inhibitors. f, Necroptosis inhibitors: necrostatin-1 (Nec-1), GSK-872, GSK-840, necrosulfonamide (NSA), and GW806742. g, Pyroptosis inhibitors: VX-765, disulfiram (DSF), dimethyl fumarate (DMF), methylcobalamin (MeCbl), and Z-VAD-FMK. h, Ferroptosis inhibitors: N-acetyl-L-cysteine (NAC), deferoxamine (DFO), liproxstatin-1 (Lip-1), and ferrostatin-1 (Fer-1). i–k, Immunoblotting of MLKL (i), GSDME (j), and NINJ1 (k) in MC38 cells deficient for Mlkl (sgMlkl), Gsdme (sgGsdme), and Ninj1 (sgNinj1), respectively...

Nature Immunology, Published online: 28 July 2026; doi:10.1038/s41590-026-02608-1Iron cleaves GSDMD

CONCLUSIONS: Our findings identify IRAK-M as an important preclinical regulator of microglial reactivity and neuroinflammatory responses in the NTG-induced chronic migraine model. IRAK-M manipulation was accompanied by bidirectional changes in TLR4/NF-κB- and NLRP3/GSDMD-relat...

Pyroptosis is an inflammatory form of regulated cell death driven by gasdermin-mediated membrane pore formation. Although gasdermin D (GSDMD) pores are widely regarded as the executioners of pyroptosis, recent studies demonstrate that pore formation is not necessarily lethal because cells can ...

Allergen exposure activates gasdermin D in lung epithelial cells through an iron-mediated, protease-independent mechanism requiring the PAR1-ferritinophagy-PCBP2 axis. This unconventional cleavage dri...