AKR1C3 Antibody (Center)
- Known as:
- AKR1C3 Antibody (Center)
- Catalog number:
- AP11656c
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- AKR1C3 Antibody (Center)
Related genes to: AKR1C3 Antibody (Center)
- Gene:
- AKR1C3 NIH gene
- Name:
- aldo-keto reductase family 1 member C3
- Previous symbol:
- HSD17B5
- Synonyms:
- KIAA0119, DDX, HAKRB, PGFS
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-29
- Date modifiied:
- 2016-10-05
Related products to: AKR1C3 Antibody (Center)
Related articles to: AKR1C3 Antibody (Center)
- Small molecule-drug conjugates (SMDCs) represent an emerging prodrug strategy for precision targeted therapy. In this study, we developed a series of cathepsin B (CTSB)-activated SMDCs targeting Aldo-keto reductase family 1 member C3 (AKR1C3). Among these conjugates, was identified as the optimized compound, which exhibited excellent inhibitory activity against AKR1C3 with an inhibitory concentration value of 9 ± 2 nM and could efficiently release the payload gemcitabine under the mediation of CTSB. The antitumor activity of was dually dependent on the expression of AKR1C3 and CTSB, allowing it to precisely recognize and eliminate tumor cells with low toxicity to normal cells. In vivo xenograft tumor assays with showed significantly superior tumor inhibitory efficacy to gemcitabine with markedly lower off-target toxicity. In conclusion, this study proposes a novel design strategy for SMDCs targeting AKR1C3, which provides a highly promising research approach to address the off-target issue in chemotherapy. - Source: PubMed
Publication date: 2026/07/18
Wang XiaolongGuo CanLiu YimengHan BingjieZhang LuLiu ZongliangChen YaoSun Haopeng - Liver cancer, particularly hepatocellular carcinoma (HCC), remains a leading cause of cancer-related mortality worldwide. Chlorogenic acid (CGA), a dietary polyphenol abundant in coffee and plant-based foods, has emerged as a potential bioactive compound with anticancer and hepatoprotective properties. This systematic review aimed to evaluate the effects of CGA on liver cancer, focusing on its molecular mechanisms and potential synergistic or antagonistic interactions. - Source: PubMed
Publication date: 2026/07/17
Pérez Amaya PérezPeña Felipe ZamoranoTorres KeilaSimón Layla - Hypercholesterolemia (HCh) represents a prevalent comorbidity in patients with diabetic foot ulcers (DFUs), frequently exacerbating wound recalcitrance, yet the mechanisms linking systemic lipid perturbation to local immune dysregulation remain poorly defined. Here, we applied an integrated transcriptomic and machine learning approach to explore the molecular basis of this comorbidity. Initial analyses identified 70 shared DEGs between DFUs and HCh, primarily enriched in pathways related to lipid homeostasis disruption and inflammatory cascade activation. Subsequently, a four-algorithm machine learning pipeline highlighted AKR1C3 and CLIC3 as candidate diagnostic biomarkers, both consistently downregulated across disease states and supported by independent external validation cohorts (AUC = 0.779 and 0.920). Immune deconvolution further indicated a dysregulated microenvironment featuring sustained innate immune activation alongside adaptive immune impairment, which correlated with reduced AKR1C3 and CLIC3 expression. Drug repurposing analyses proposed that pirfenidone and statins might attenuate this pathological transcriptomic signature, while molecular docking simulations suggested stable binding of exemestane and indomethacin to AKR1C3 (binding energies: -8.0 and -7.3 kcal/mol, respectively). Collectively, these findings suggest that AKR1C3 and CLIC3 act as molecular bridges linking the TGF-β/lipid metabolism axis to local immune dysfunction, offering a rationale for early risk stratification and targeted drug repurposing in DFUs-HCh comorbidity. - Source: PubMed
Publication date: 2026/07/13
Xu YueyuanLi YoushanWu Chunyuan - Sulfonylureas (SUs) have been used in the treatment of type 2 diabetes since the 1950s, yet growing evidence shows that many members of this class also exert biologically relevant off-target effects that may be exploited in oncology and other therapeutic contexts. This review provides a structured overview of the literature from 1956 to 2025, integrating preclinical studies, clinical and epidemiological data, pharmacovigilance signals, and patent activity. To facilitate comparison across compounds, the available evidence is organized into drug-specific mechanistic maps rather than treated as a uniform class effect. Across the literature, SUs have been linked to modulation of K channels, ABC transporters involved in multidrug resistance, gap-junction communication, redox balance, mitochondrial function, inflammatory signaling, and DNA damage-related pathways. However, these activities differ markedly between individual agents. Glibenclamide emerges primarily as a chemosensitizing and transporter-modulating compound, gliclazide as a drug with antioxidant, anti-inflammatory, and DNA-protective properties, glimepiride as a promising synergistic agent with additional AKR1C3-inhibitory activity, tolbutamide as a modulator of gap-junction signaling and mitochondrial stability, and chlorpropamide derivatives as ALDH-targeting chemosensitizers. At the same time, the review highlights major translational constraints, including weak baseline cytotoxicity for most SUs, frequent exposure mismatches between experimental and clinical settings, heterogeneous safety profiles, photoreactivity, and limited commercial incentives for development, while also outlining practical strategies to address these limitations. Overall, SUs should not be viewed as a single repurposing candidate, but as a chemically related set of drugs that require indication-specific and compound-specific selection for future oncology applications. - Source: PubMed
Publication date: 2026/06/06
Tomczyk Mateusz DWawrzynosek ClaudiaGendosz de Carrillo DariaKrzystanek MarekPantziarka PanJędrzejowska-Szypułka Halina - Hyperandrogenism during childhood is a key feature of several pediatric endocrine disorders, including premature adrenarche and polycystic ovary syndrome (PCOS). The adrenal gland contributes significantly to circulating androgens, yet the regulation of adrenal steroidogenic enzymes during the prepubertal period remains poorly understood. This study aimed to investigate adrenal androgen synthesis in a prepubertal rat model of ovarian removal and identify key enzymes responsible for hyperandrogenism. - Source: PubMed
Publication date: 2026/05/27
Gao GuanglinWang JunqiZhan BowenLi BowenShao YanyanHan XinghuiHe JingweiSun WenYu JianDong Wenke