Cell Death

Cell death programs—apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy-coupled death—shape development, homeostasis, and disease. We provide marker antibodies (Caspase, PARP, Bcl-2 family, RIPK–MLKL, GSDMD, GPX4, etc.) and chemical probes across apoptosis/necroptosis/ferroptosis/inflammasome axes for mechanistic and phenotypic studies.

Focus areas: mitochondrial apoptosis & MOMP, death-receptor signaling, necrosome & membrane rupture, inflammasome–GSDMD axis, lipid peroxidation & ferroptosis

Cell death–related antibodies (curated)

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Hot topics & directions

  • Apoptosis & drug resistance: Bcl-2 network & MOMP thresholds setting therapeutic windows.
  • Necroptosis & inflammation: RIPK3–MLKL-dependent DAMP release amplifying tissue injury.
  • Pyroptosis & infection immunity: Inflammasome–caspase-1/11–GSDMD in infection vs sepsis.
  • Ferroptosis & metabolic disease: Lipid remodeling, iron homeostasis, GPX4 axis druggability in cancer/neurodegeneration.

Related targets

Intrinsic apoptosis (mitochondria)
BAX, BAK, BCL2, BCL-XL, MCL1, BAD, BIM, PUMA, NOXA, cytochrome c, APAF1, caspase-9
Extrinsic apoptosis (death receptors)
FAS, FASL, TNFRSF1A, TRAIL (TNFSF10), TRADD, FADD, caspase-8/10, c-FLIP
Necroptosis
RIPK1, RIPK3, MLKL, PGAM5 (context), AIFM1 (parthanatos-related reads)
Pyroptosis / ferroptosis
NLRP3, caspase-1/4/5/11 (species-dependent), GSDMD, GPX4, ACSL4, SLC7A11

Key signaling pathways

  1. BCL-2 family → MOMP → apoptosome → caspase-3/7
    MOMP is a major execution node; separate early vs late apoptosis readouts.
  2. TNF / TRAIL → complex I/II → caspase-8 / RIPK1 switch
    One receptor platform toggles apoptosis/necroptosis/survival via cIAPs, RIPK1 ubiquitination, c-FLIP.
  3. RIPK1–RIPK3–MLKL → membrane rupture
    MLKL oligomerization drives regulated necrosis; distinguish from accidental necrosis.
  4. Inflammasome → caspase-1 → GSDMD pores → IL-1β release
    Pyroptosis couples to inflammation; mind species differences for caspase-4/5/11.
  5. GPX4 / lipid peroxidation / iron
    PUFA lipid peroxidation defines ferroptosis; crosstalk with mitochondria and autophagy flux.

Tool compounds (research use)

Commonly used for mechanistic studies; follow your lab SOP, compound datasheets, and ethics approvals.

CompoundTargets / pathwaysExperimental notes
Z-VAD-FMKCaspases (broad)Classic apoptosis blockade; mind off-target toxicity—pair vehicle controls and time courses.
Q-VD-OPhCaspases (context-dependent preference)Often better tolerated than Z-VAD in vitro; pair with cleaved PARP/caspase and membrane integrity.
Necrostatin-1 (Nec-1)RIPK1 kinase activityCommon necroptosis tool; mind isoforms/off-targets—cross-validate with genetics.
Ferrostatin-1 (Fer-1)Lipid peroxidation / ferroptosis (radical trapping; context-dependent)Pair with GPX4/ACSL4/lipidomics; separate ferroptosis from other oxidative death phenotypes.
Liproxstatin-1Ferroptosis (potent lipophilic antioxidant; model-dependent)Often paired with Erastin/RSL3 induction; mitochondria/autophagy can confound.
MCC950NLRP3 inflammasomeUpstream of pyroptosis; pair with GSDMD cleavage and IL-1β release readouts.
ErastinSystem Xc⁻ / ferroptosis induction (tool use)Induces ferroptosis models—not cytoprotective; pair with Fer-1/Liproxstatin rescue.