Nicotinamide adenine dinucleotide, a coenzyme critical for cellular energy metabolism that declines with age. NAD+ precursors like NMN and NR are studied as longevity interventions.

Mechanistic target of rapamycin, a key nutrient-sensing pathway that regulates cell growth and aging. Inhibiting mTOR (e.g., with rapamycin) has shown lifespan extension in multiple organisms.

A class of drugs that selectively eliminate senescent (aged, dysfunctional) cells to reduce inflammation and improve tissue function.

What is Epigenetic clock?

A biomarker based on DNA methylation patterns that estimates biological age, often more predictive of health outcomes than chronological age.

The period of life spent in good health, free from chronic diseases and disability associated with aging.

An immunosuppressant drug that inhibits the mTOR pathway. Research shows rapamycin may extend lifespan and improve age-related health outcomes in multiple species.

What is Biological age?

A measure of how well or poorly your body is functioning relative to your chronological age, assessed through biomarkers such as DNA methylation, telomere length, and blood panels.

What is Caloric restriction?

A dietary regimen that reduces calorie intake without malnutrition. Caloric restriction is one of the most studied interventions shown to extend lifespan across species.

Protective caps at the ends of chromosomes that shorten with each cell division. Telomere length is associated with aging and age-related diseases.

A state in which cells permanently stop dividing but resist death, accumulating with age and secreting inflammatory factors that damage surrounding tissue.

A second-generation epigenetic clock that predicts time to death and is considered one of the most accurate measures of biological aging.

What is Inflammaging?

Chronic, low-grade inflammation that increases with age and contributes to the development of age-related diseases including cardiovascular disease, diabetes, and neurodegeneration.

The large-scale study of proteins in biological systems. In longevity research, proteomics identifies blood protein signatures that predict biological age and disease risk.

What is Yamanaka factors?

A set of four transcription factors (Oct4, Sox2, Klf4, c-Myc) that can reprogram adult cells to a pluripotent state. Partial reprogramming with Yamanaka factors is being explored to reverse cellular aging.

Nicotinamide mononucleotide, a precursor to NAD+ that is widely studied as a supplement to boost cellular energy and combat age-related decline.

A gene-editing technology that allows precise modifications to DNA. In longevity research, CRISPR is used to study and potentially modify genes associated with aging.

Amphista Therapeutics presents the discovery, characterisation and chemical structure of AMX-883, an orally bioavailable, highly potent and selective DCAF16 degrader of BRD9 at AACR 2026

Amphista Therapeutics has publicly disclosed the chemical structure of AMX-883, a novel DCAF16-dependent Targeted Glue™ degrader of BRD9, during the AACR Annual Meeting 2026. This orally bioavailable compound is the company’s lead asset and is set to enter a Phase I clinical trial for acute myeloid leukaemia (AML) in the second half of 2026. The presentation highlighted the discovery and optimization of AMX-883, showcasing its picomolar potency and selectivity over related bromodomain proteins, BRD4 and BRD7, confirmed through high-resolution cryo-EM structural analysis.

The significance of AMX-883 lies in its potential to address a critical unmet need in AML treatment. By degrading BRD9, AMX-883 alleviates the differentiation block that characterizes AML, promoting the expression of myeloid differentiation genes while repressing pro-proliferative pathways. Preclinical data indicate that AMX-883 enhances myeloid maturation markers across diverse AML cell lines, including those with TP53 mutations. Furthermore, it demonstrates robust efficacy as a monotherapy in blocking tumor growth in vivo and shows synergistic effects when combined with venetoclax, effectively preventing resistance—a major challenge in AML therapy.

The introduction of AMX-883 could shift current paradigms in AML research and treatment. Its karyotype-independent mechanism positions it as a broadly applicable therapeutic option, potentially benefiting a wider patient population than existing treatments. This advancement underscores the promise of Targeted Glue™ degraders in oncology, paving the way for innovative strategies in drug development and enhancing the therapeutic landscape for aggressive blood cancers like AML.

Source: globenewswire.com