673-a

673-A is an aldehyde dehydrogenase (ALDH1A) inhibitor that depletes CD133+ cancer stem cells (CSC) in ovarian cancer cell lines. 673-A triggers necroptosis in ovarian CSCs and induces expression of mitochondrial uncoupling proteins (UCP). 673-A also overcomes chemotherapy resistance in vivo.

Talazoparib (LT-673) is a new-type PARP inhibitor (IC50: 0.58 nM), It similarly binds to PARP1/2 (Kis: 1.2/0.85 nM).

CM-675 is a dual inhibitor of phosphodiesterase 5 (PDE5) and class I histone deacetylases (IC50s: 114 nM and 673 nM for PDE5 and HDAC1) with the potential to treat Alzheimer's disease.

Compound Fr13871, with CAS No. 673-66-5, is a fragment molecule that serves as an important scaffold for molecular linking, expansion, and modification. Compound Fr13871 provides a structural basis and research tool for the design and screening of novel drug candidates, and is commonly used in drug discovery, drug synthesis, and related research.

Amyloid-β (1-8, A2V) is a truncated form of amyloid-β (Aβ) that contains a valine to alanine substitution at position 2 of the Aβ numbering convention (Aβ A2V), which corresponds to position 673 of the amyloid precursor protein (APP) numbering convention (APP A673V). An Aβ (1-40) (Aβ40) A2V peptide increases the production of Aβ and the rate and amount of amyloid fibril formation in vitro, effects that can be reduced by coincubation with wild-type Aβ40. Aβ40 and Aβ42 levels are increased in CHO cells expressing the Aβ A2V mutation and in fibroblasts derived from patients with the Aβ A2V mutation. As a homozygous mutation, Aβ A2V is correlated with Alzheimer's disease with distinctive pathological features, but disease does not develop in patients with a heterozygous Aβ A2V mutation.

MY-673, a colchicine binding site inhibitor (CBSI), impedes tubulin polymerization and disrupts the ERK signaling pathway, consequently modulating SMAD4 protein expression in the TGF-β/SMAD pathway. This compound effectively reduces cell proliferation and migration while inducing apoptosis in both in vivo and in vitro settings [1].

Emerfetamab (AMG 673) is a dual-specificity T-cell engager (bispecific T-cell engager) with an extended half-life that targets both CD33 and CD3. By redirecting T cells towards CD33+ cells, Emerfetamab induces T-cell mediated cytotoxicity against progenitor cells in acute myeloid leukemia (AML).