AKR1C3 (Human) Recombinant Protein (P01)
- Known as:
- AKR1C3 (Human) Recombinant Protein (P01)
- Catalog number:
- H00008644-P01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- AKR1C3 (Human) Recombinant Protein (P01)
Related genes to: AKR1C3 (Human) Recombinant Protein (P01)
- 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
- Gene:
- BZW2 NIH gene
- Name:
- basic leucine zipper and W2 domains 2
- Previous symbol:
- -
- Synonyms:
- HSPC028, MST017, MSTP017
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-05
- Date modifiied:
- 2016-10-05
- Gene:
- C2CD3 NIH gene
- Name:
- C2 calcium dependent domain containing 3
- Previous symbol:
- -
- Synonyms:
- DKFZP586P0123
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2007-10-17
- Date modifiied:
- 2016-06-08
- Gene:
- MBTD1 NIH gene
- Name:
- mbt domain containing 1
- Previous symbol:
- -
- Synonyms:
- SA49P01, FLJ20055
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-15
- Date modifiied:
- 2015-04-21
- Gene:
- TMEM63C NIH gene
- Name:
- transmembrane protein 63C
- Previous symbol:
- C14orf171
- Synonyms:
- DKFZp434P0111, CSC1, hsCSC1
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-10
- Date modifiied:
- 2017-10-17
Related products to: AKR1C3 (Human) Recombinant Protein (P01)
Related articles to: AKR1C3 (Human) Recombinant Protein (P01)
- 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 - Aldo-keto reductase family 1 member C3 (AKR1C3) is a pivotal metabolic enzyme involved in arachidonic acid (AA) metabolism and cancer metabolic reprogramming, which plays a critical role in the initiation and progression of glioblastoma (GBM). We integrated single-cell and transcriptome data to characterize AA metabolism features in GBM and identify the key gene AKR1C3. Using CCK8 assays, wound-healing assays, transwell assays, and mouse tumor formation experiments, we elucidated the effects of AKR1C3. Dual-luciferase reporter assays and ChIP-PCR experiments were performed to investigate the regulation of transcription factor JUN on AKR1C3 expression. RNA-seq analysis, combined with rescue experiments, demonstrated that AKR1C3 significantly regulates the RhoA/ROCK pathway. Arachidonic acid metabolism is closely associated with clinical outcomes in glioma, with AKR1C3 identified as a key gene within this pathway. AKR1C3 knockdown enhanced tumor cell proliferation, migration, and invasion, whereas AKR1C3 overexpression suppressed these malignant behaviors. In vivo experiments further confirmed the inhibitory effect of AKR1C3 on glioma progression. Dual-luciferase reporter and ChIP-PCR assays demonstrated that JUN acts as an upstream regulator of AKR1C3. ELISA results indicated that AKR1C3 overexpression reduced cellular PGD2 levels. RNA-seq analysis suggested that the RhoA/ROCK pathway was a downstream effector of AKR1C3, and exogenous PGD2 supplementation could reverse AKR1C3-mediated regulation of this pathway. We identified curcumin, a natural product with anti-cancer metabolic regulatory activity, as an upstream modulator that suppresses JUN expression, thereby activating the JUN/AKR1C3 axis and inhibiting malignant phenotypes in GBM cells. JUN/AKR1C3 axis influences glioma progression via modulating PGD2-mediated RhoA/ROCK Signaling. - Source: PubMed
Publication date: 2026/07/03
Wang JieMa HuihaoFeng BaozhiFu YanLu ChunlinFei MingyangZhang YuxinDong BinLi YingLiu Jing - Aldo-keto reductase 1C3 (AKR1C3) is a drug target for the treatment of various androgen dependent malignancies, including castration-resistant prostate canceras well as hematological cancers. The enzyme plays a key role in the conversion of androgen precursors into potent androgen receptor ligands and the conversion of prostaglandins from pro-differential to pro-proliferative, facilitating progression of these malignancies. Additionally, AKR1C3 plays a role in chemotherapy resistance, reducing therapeutics to inactive forms and stabilizing expression of mutant androgen receptors. - Source: PubMed
Publication date: 2026/07/03
Case Alfie MSmith Melanie MMack Cole ATrippier Paul C - OBI-3424 is an investigational small molecule prodrug. In a dose-escalation trial, the OBI-3424 recommended phase 2 dose (RP2D) was 12 mg/m2 administered every 21 days. In this phase 2 dose-expansion trial, we evaluated the safety and efficacy of OBI-3424 in pancreatic adenocarcinoma and other solid tumor types ("basket" cohort). - Source: PubMed
Publication date: 2026/07/02
Tsimberidou Apostolia MariaVerschraegen ClaireSigal DarrenLenz Heinz-JosefHochster HowardBaysal Mehmet AChakraborty AbhijitLee InglyRistoski KoenuelXu Dong