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BioWorld - Friday, May 8, 2026
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Transmission electron micrograph of HIV particles
HIV/AIDS

DOT1L/H3K79me2 recruits DCAF1 to establish a negative feedback loop restricting HIV-1 reactivation

Aug. 23, 2024
In mammals, the disruptor of telomeric silencing 1-like (DOT1L) is the only methyltransferase that catalyzes the mono-, di- and tri-methylation of histone H3 at lysine 79 (H3K79). The DOT1L/H3K79me is involved in several relevant physiological and pathological mechanisms, including several viral infections.
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Dermatologic

Azitra gains IND clearance for ATR-04 for EGFR inhibitor-associated dermal toxicity

Aug. 23, 2024
Azitra Inc. has obtained IND clearance from the FDA for a first-in-human phase I/II study of ATR-04 for moderate to severe EGFR inhibitor-associated dermal toxicity. The study is expected to begin by year-end.
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Tau protein in Alzheimer's disease
Neurology/psychiatric

IGC Pharma’s IGC-1C shown to target tau protein and GLP-1 receptor

Aug. 23, 2024
IGC Pharma Inc. has reported preclinical research demonstrating the therapeutic potential of IGC-1C, a cyclic dipeptide-based small-molecule modulator, in neurodegenerative disease due to its modulation of tau protein, which is involved in the formation of neurofibrillary tangles, a key hallmark of Alzheimer’s disease.
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Scientist looking in microscope, chemical structure concept image
Cancer

Simcere’s POLθ inhibitor to enter clinic in China for advanced solid tumors

Aug. 23, 2024
Simcere Zaiming Pharmaceutical Co. Ltd. has obtained clinical trial approval from China’s National Medical Products Administration (NMPA) for SIM-0508, a small-molecule inhibitor of DNA polymerase θ (POLθ), allowing initiation of clinical trials in locally advanced or metastatic solid tumors.
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Art concept for hematologic cancer
Cancer

Identification of highly potent, orally bioavailable BCL6 ligand-directed degraders

Aug. 23, 2024
At the recently concluded ACS Fall meeting, Bristol Myers Squibb Co. reported the discovery of potent orally bioavailable B-cell lymphoma 6 protein (BCL6) ligand-directed degraders (LDDs).
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Gastrointestinal

SOX7 plays key role in liver fibrosis by regulating hepatic stellate cell activation

Aug. 23, 2024
The activation of hepatic stellate cells (HSCs) is a key process in the pathogenesis of liver fibrosis, but the molecular mechanisms behind it are not fully understood. By combining the analysis of differentially expressed gene screening of HSC transcriptome and weighted gene coexpression network analysis of liver tissue, researchers searched for transcription factors involved in liver fibrosis.
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3D cross-section illustration of muscle anatomy
Neurology/psychiatric

Ractigen’s saRNA therapeutic named US orphan drug for Duchenne and Becker muscular dystrophies

Aug. 23, 2024
Ractigen Therapeutics Co. Ltd.’s small activating RNA (saRNA) therapeutic, RAG-18, has been awarded U.S. orphan drug designation for the treatment of Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy.
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Vial and syringe
Infection

Universal flu vaccine candidate successfully tested in animals

Aug. 23, 2024
The efficacy of seasonal flu vaccines varies due to the ability of the influenza virus to mutate rapidly. The achievement of a universal flu vaccine conferring protection against all strains, including those with pandemic potential, for longer than a single season would provide a great benefit and has not yet been achieved.
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Kelin Zhao and Daniel Gray
Aging

Discovery of new age-related epithelial cells sheds light on aging in the thymus

Aug. 23, 2024
By Tamra Sami
Researchers at the Walter and Eliza Hall Institute of Medical Research (WEHI) in Melbourne have discovered new cells that drive the aging process in the thymus that could unlock a way to restore function and prevent immunity from waning as we age. The thymus is the first organ in the body to shrink as people age. As this happens, the T-cell growth areas in the thymus are replaced with fatty tissue, diminishing T-cell production and contributing to a weakened immune system.
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Gamma secretase protein complex
Neurology/psychiatric

Presenilin mutations kill neurons, no amyloid-β required

Aug. 23, 2024
By Mar de Miguel
Scientists at Harvard Medical School have shown that in mice lacking amyloid beta (Aβ), the fundamental hallmark of Alzheimer's disease (AD), neurons died from the effect of the most harmful mutation of this neurodegenerative disease. They showed that presenilin (PS) could be behind the origin of the disease without the need for Aβ. They maintain that it is time to update theories and redirect efforts.
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