CAS 437-64-9 Genkwanin - Analytical Products / Alfa Chemistry

CAT	APS437649
CAS	437-64-9
Structure
MDL Number	MFCD00017452
Synonyms	Genkwanin (6CI), 5,4'-Dihydroxy-7-methoxyflavone, 7-O-Methylapigenin, Apigenin 7-O-methyl ether, 7-Methylapigenin,4H-1-Benzopyran-4-one, 5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-, Flavone, 4',5-dihydroxy-7-methoxy- (7CI,8CI), 5-Hydroxy-2-(4-hydroxyphenyl)-7-methoxy-4H-1-benzopyran-4-one, 4',5-Dihydroxy-7-methoxyflavone, Apigenin 7-methyl ether, Puddumetin
IUPAC Name	5-hydroxy-2-(4-hydroxyphenyl)-7-methoxychromen-4-one
Molecular Weight	284.26
Molecular Formula	C16H12O5
Canonical SMILES	COc1cc(O)c2C(=O)C=C(Oc2c1)c3ccc(O)cc3
InChI	InChI=1S/C16H12O5/c1-20-11-6-12(18)16-13(19)8-14(21-15(16)7-11)9-2-4-10(17)5-3-9/h2-8,17-18H,1H3
InChI Key	JPMYFOBNRRGFNO-UHFFFAOYSA-N
REAXYS Number	292549

Description	analytical standard
Accurate Mass	284.0685
Assay	≥98.0% (HPLC)
Format	Neat
Grade	analytical standard
Shipping	Room Temperature
Size	10MG
Storage Conditions	-20°C Freezer
Subcategory	Food additives, flavours and adulterants

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Case Study

Genkwanin Is Used to Attenuate Intervertebral Disc Degeneration via ITGA2/PI3K/AKT, NF-κB, and MAPK Pathways

Li, Mengwei, et al. International Immunopharmacology 133 (2024): 112101.

Genkwanin, a naturally occurring flavonoid known for its anti-inflammatory properties, has demonstrated significant therapeutic potential in the treatment of intervertebral disc degeneration (IVDD). In this study, a combination of in vitro and in vivo experiments was conducted to assess the pharmacological mechanisms of genkwanin.
In vitro, nucleus pulposus (NP) cells were pre-treated with various concentrations of genkwanin and stimulated with interleukin-1β (IL-1β) to induce inflammation. The results revealed that genkwanin inhibited the expression of key inflammatory mediators including IL-6, iNOS, and COX-2, while suppressing matrix degradation by downregulating MMP-13. At the same time, genkwanin upregulated extracellular matrix components such as aggrecan and type II collagen. Mechanistic studies showed that genkwanin inhibited the phosphorylation of PI3K/AKT/mTOR, MAPK, and NF-κB signaling pathways.
Transcriptomic analysis further identified integrin α2 (ITGA2) as a potential target of genkwanin, with silencing of ITGA2 reversing PI3K/AKT pathway activation. Additionally, genkwanin treatment alleviated IL-1β-induced cellular senescence and apoptosis in NP cells.
In vivo, administration of genkwanin in a rat IVDD model resulted in significant structural preservation of intervertebral discs, as confirmed by imaging and histological analysis.
Overall, this study highlights that genkwanin is used to attenuate IVDD by targeting inflammatory and catabolic pathways, supporting its potential as a therapeutic candidate for early-stage disc degeneration.

Genkwanin Is Used to Promote Osteogenic Differentiation and Prevent Bone Loss via the pJNK-NFATc1 Pathway

Hao, Yu-Xuan, et al. European Journal of Pharmacology (2025): 177687.

Genkwanin (GWA), a flavonoid compound derived from traditional Chinese medicinal plants, has shown promising effects in bone regenerative applications. This study systematically investigated the role of GWA in promoting osteogenic differentiation and its therapeutic potential against osteoporosis.
In vitro, bone marrow-derived mesenchymal stem cells (BMSCs), MC3T3-E1 pre-osteoblasts, and human BMSCs (hBMSCs) were exposed to GWA under osteogenic induction conditions. GWA significantly enhanced mineralized nodule formation in a dose- and time-dependent manner. Flow cytometry confirmed the high purity of BMSCs (>90% CD90⁺/CD44⁺), ensuring reliable osteogenic assays. Cytotoxicity analysis demonstrated GWA was non-toxic up to 20 μM in BMSCs and 10 μM in MC3T3-E1 cells.
Mechanistically, GWA was found to directly bind phosphorylated JNK (pJNK), thereby preventing the phosphorylation and cytoplasmic retention of NFATc1. This promoted NFATc1 nuclear translocation, enhancing transcription of osteogenic markers such as COL1A1. Notably, this regulatory mechanism is distinct from the canonical JNK/AP-1/NFATc1 pathway known to activate osteoclastogenesis.
In vivo, an ovariectomized (OVX) mouse model confirmed that GWA administration effectively reduced bone loss and preserved COL1A1 expression without activating estrogen-related pathways, minimizing the risk of hormone-sensitive side effects.
These findings suggest Genkwanin is used to promote osteoblast differentiation and bone matrix production by modulating the pJNK-NFATc1 axis, offering a novel, non-estrogenic therapeutic strategy for osteoporosis and other bone-loss conditions.

Genkwanin Is Used for Attenuating Neuroinflammation and Neurotoxicity via TLR4/MyD88/NLRP3 Pathway in Parkinson's Disease Models

Li, Qiang, Peilan Zhang, and Yun Cai. Neurotoxicology 87 (2021): 62-69.

Genkwanin, a non-glycosylated flavonoid with recognized anti-inflammatory and antioxidant activities, has shown therapeutic promise in neurodegenerative diseases. This study systematically evaluated its neuroprotective effects in a cellular model of Parkinson's disease (PD) using MPP⁺-treated SH-SY5Y cells.
In vitro assays demonstrated that genkwanin (≤40 μM) exhibited no cytotoxicity, maintaining cell viability and suppressing lactate dehydrogenase (LDH) release. MPP⁺ exposure induced significant oxidative stress, mitochondrial dysfunction, apoptosis (evidenced by caspase-3/7 activity and TUNEL staining), and robust neuroinflammation marked by elevated PGE2, TNF-α, IL-1β, and IL-6. These pathological changes were dose-dependently reversed by genkwanin treatment.
Mechanistic investigation revealed that genkwanin inhibited activation of the TLR4/MyD88/NLRP3 inflammasome signaling cascade, a key inflammatory axis implicated in PD progression. Western blot analysis showed genkwanin markedly suppressed MPP⁺-induced expression of COX-2, TLR4, MyD88, and NLRP3 proteins. Furthermore, TLR4 overexpression weakened the anti-neurotoxic and anti-inflammatory effects of genkwanin, confirming TLR4 pathway involvement.
Overall, genkwanin is used for attenuating neuroinflammation and neuronal injury by targeting the TLR4/MyD88/NLRP3 pathway in MPP⁺-induced PD models. These findings suggest genkwanin holds significant potential as a therapeutic candidate for neuroinflammatory components of Parkinson's disease and possibly other neurodegenerative disorders involving innate immune activation.