Over the course of the year, and continuing into the latest scientific meetings, an extraordinary breadth of new antibody-drug conjugate (ADC) designs was reported, with innovations spanning targets, linkers, payloads, conjugation chemistries and overall architectures. Once defined by a simple “one target, one payload” model, the field is lately expanding into a more versatile and diverse therapeutic space.
Over the course of the year, and continuing into the latest scientific meetings, an extraordinary breadth of new antibody-drug conjugate (ADC) designs was reported, with innovations spanning targets, linkers, payloads, conjugation chemistries and overall architectures. Once defined by a simple “one target, one payload” model, the field is lately expanding into a more versatile and diverse therapeutic space.
Fat tissue balances energy by storing lipids during times of abundance and mobilizing them when needed, yet sustained metabolic stress demands mechanisms that limit excessive lipid loss. Researchers at the University of California San Diego (UCSD) report that stress-induced fat breakdown triggers a neutrophil response in visceral adipose tissue that feeds back to restrain lipolysis and preserve lipid reserves.
Fat tissue balances energy by storing lipids during times of abundance and mobilizing them when needed, yet sustained metabolic stress demands mechanisms that limit excessive lipid loss. Researchers at the University of California San Diego (UCSD) report that stress-induced fat breakdown triggers a neutrophil response in visceral adipose tissue that feeds back to restrain lipolysis and preserve lipid reserves.
NIH researchers report that in severe influenza, survival improves at late stages only when antivirals are combined with therapies that repair lung damage or limit harmful T-cell responses, explaining why anti-inflammatory treatments alone are often ineffective.
NIH researchers report that in severe influenza, survival improves at late stages only when antivirals are combined with therapies that repair lung damage or limit harmful T-cell responses, explaining why anti-inflammatory treatments alone are often ineffective.
Researchers from the Chinese Institute for Brain Research, the Chinese Academy of Medical Sciences, and their collaborators have identified adenosine as the driving force behind the rapid, fast-acting antidepressant effects of ketamine and electroconvulsive therapy (ECT). “Our journey into this area of research began over a decade ago, around 2013, when the clinical world was buzzing with excitement about ketamine's remarkably rapid antidepressant effects,” Minmin Luo, co-senior author of the study, told BioWorld.
Researchers from the Chinese Institute for Brain Research, the Chinese Academy of Medical Sciences, and their collaborators have identified adenosine as the driving force behind the rapid, fast-acting antidepressant effects of ketamine and electroconvulsive therapy (ECT). “Our journey into this area of research began over a decade ago, around 2013, when the clinical world was buzzing with excitement about ketamine's remarkably rapid antidepressant effects,” Minmin Luo, co-senior author of the study, told BioWorld.
Blocking progesterone receptor (PR) activity has long been viewed as a possible approach to breast cancer prevention. Historically, most supporting evidence came from animal models, epidemiological studies or mechanistic pathway analyses. Now, a team at the University of Manchester has uncovered direct mechanistic and clinical evidence that PR antagonists can reprogram the breast tissue microenvironment, suggesting a novel avenue for reducing breast cancer risk in women.
At the AACR-NCI-ORTC conference, researchers from Dewpoint Therapeutics Inc. presented advances in targeting MYC condensates, revealing a potential breakthrough strategy for treating cancers driven by MYC – a well-established oncogenic driver that is frequently overexpressed or amplified across a range of human cancers.
