Anti-aging

Anti-aging research spans cellular senescence programs, telomeric and epigenetic stability, nutrient sensing (mTOR/AMPK), proteostasis, and chronic inflammation. We provide antibodies and small-molecule tools for SIRT pathways, senescence markers, autophagy, and mitochondrial stress to support aging biology and intervention studies.

Focus areas: senescent cells & SASP, NAD+ metabolism, mTOR–autophagy axis, DDR, stem-cell exhaustion & niche remodeling

Anti-aging-related antibodies (curated)

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Hot topics & directions

  • Cellular senescence & SASP: p16/p21/p53 axis and secretory phenotypes impacting tissue homeostasis and bystander effects.
  • Nutrient sensing & reprogramming: mTORC1, AMPK, and mitochondrial biogenesis/clearance balance across age.
  • NAD+ & sirtuin axis: Tissue-specific roles of NAD+ consumers (CD38/PARP) vs biosynthetic routes.
  • Proteostasis & multimorbidity: Declining UPS–autophagy–lysosome function coupling to neurodegenerative/metabolic risk.

Related targets

Senescence markers & CDKIs
CDKN2A (p16INK4a), CDKN1A (p21), TP53, RB1, HMGB1 (DAMP context)
Longevity & stress response
SIRT1/3/6, FOXO3, KL, NAMPT, CD38, PARP1
Telomeres & genome maintenance
TERT, TERF1/2, POT1, ATM/ATR axis, γH2AX
Autophagy & mitochondrial QC
MTOR, PRKAA1/2, ULK1, BECN1, PINK1, PRKN (Parkin)

Key signaling pathways

  1. IGF-1–PI3K–AKT–FOXO
    Nutrient-sensing longevity branch; extensive crosstalk with mTORC1.
  2. AMPK ↔ mTORC1
    Canonical antagonism linking energy deficit to autophagy initiation.
  3. DDR–p53–p21 & senescence entry
    Replicative/telomeric stress can trigger stable arrest—separate reversible arrest vs senescence.
  4. NAD+ salvage / CD38 / PARP consumption
    Inflammation/DDR can accelerate NAD+ decline—tissue-specific readouts matter.

Tool compounds (research use)

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

CompoundTargets / pathwaysExperimental notes
RapamycinmTORC1 (FKBP12–Raptor)Common for aging/autophagy studies; chronic dosing may engage mTORC2 feedback.
Torin 1mTORC1 / mTORC2 (ATP-competitive; concentration-dependent)Broader mTOR inhibition than rapamycin—tight dose windows and controls required.
AICARAMPK-activating tool compoundEnergy-stress readouts; pair with phospho-AMPK/downstream ACC validation.
Compound CAMPK (tool antagonist; promiscuous)Use as dependency controls; promiscuous—avoid over-interpreting single doses.
ResveratrolSIRT1 and other targets (debated)Literature-rich but pleiotropic; use dose/time matrices and vehicle controls.
OlaparibPARP1/2DDR/synthetic lethality contexts; cell-type and cell-cycle dependent in aging models.
MG132ProteasomeProteostasis/turnover studies; high cytotoxicity—window doses tightly.