tbResList Print — CHr Chrysin

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CHr Chrysin
Description: <b>Chrysin</b> is found in passion flower and honey. It is a flavonoid.<br>
-To reach plasma levels that might more closely match the concentrations used in in vitro studies (typically micromolar), considerably high doses or advanced delivery mechanisms would be necessary.<br>

Chrysin is widely summarized as modulating PI3K/Akt and MAPK pathways in cancer.<br>
<br>


<p><b>Chrysin</b> — Chrysin is a naturally occurring flavone-class flavonoid found in honey, propolis, passionflower, and several plants. Its oncology relevance is mainly preclinical: it shows multi-pathway anticancer activity in cell and animal models, but native oral chrysin has very poor systemic bioavailability and no established approved oncology use.</p>

<p><b>Primary mechanisms (ranked):</b></p>
<ol>
<li>Suppression of PI3K/AKT survival signaling with downstream reduction in proliferation and survival programs.</li>
<li>Induction of mitochondrial apoptosis through Bax/Bcl-2 shift, mitochondrial membrane potential loss, cytochrome c release, and caspase activation.</li>
<li>Context-dependent ROS stress amplification in cancer cells, often linked to mitochondrial injury, ER stress, and apoptosis.</li>
<li>ER stress / unfolded-protein-response activation leading to autophagy or stress-to-death coupling.</li>
<li>Suppression of inflammatory, invasive, angiogenic, and metastatic signaling including NF-κB, MMPs, EMT, VEGF, and HIF-1α axes.</li>
<li>Secondary antioxidant / NRF2-linked cytoprotection in some normal-cell or injury models, which is context-dependent and not necessarily anticancer-selective.</li>
</ol>

<p><b>Bioavailability / PK relevance:</b> Native oral chrysin has very poor systemic exposure because of low aqueous solubility, extensive intestinal/hepatic glucuronidation and sulfation, and efflux; human oral bioavailability has been reported as extremely low, often summarized as below 1%. Formulation strategies such as nanoparticles, lipid systems, micelles, cyclodextrins, or structural analogues are commonly proposed for systemic translation.</p>

<p><b>In-vitro vs systemic exposure relevance:</b> Most anticancer studies use micromolar in-vitro concentrations that are unlikely to be reached in plasma after ordinary oral chrysin. Local intestinal exposure may be more plausible than systemic tumor exposure, but systemic anticancer claims should be treated as formulation-dependent. <br>
<a href="https://www.mdpi.com/2076-3921/14/11/1313#app1-antioxidants-14-01313">LipoMicel</a> may increase bioavailability
</p>

<p><b>Clinical evidence status:</b> Preclinical. Evidence is strong enough for mechanistic oncology interest in cell and animal models, including combination/sensitization studies, but there is no mature clinical oncology evidence establishing therapeutic benefit.</p>



-Note <a href="tbResList.php?qv=61&tsv=1109&wNotes=on&exSp=open">half-life</a> 2 hrs,
<a href="tbResList.php?qv=61&tsv=792&wNotes=on&exSp=open">BioAv</a> very poor often <1%
<br>
Pathways:<br>
<a href="https://cancerci.biomedcentral.com/articles/10.1186/s12935-021-01906-y/figures/3">Graphical Pathways</a><br>
<br>
<!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑-->
- may induce
<a href="tbResList.php?qv=61&tsv=275&wNotes=on">ROS</a> production<br>
- ROS↑ related:
<a href="tbResList.php?qv=61&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm),
<a href="tbResList.php?qv=61&tsv=103&wNotes=on">ER Stress↑</a>,
<a href="tbResList.php?qv=61&tsv=459&wNotes=on">UPR↑</a>,
<a href="tbResList.php?qv=61&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=61&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>,
<a href="tbResList.php?qv=61&tsv=77&wNotes=on">Cyt‑c↑</a>,
<a href="tbResList.php?qv=61&wNotes=on&word=Casp">Caspases↑</a>,
<a href="tbResList.php?qv=61&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>,
<a href="tbResList.php?qv=61&tsv=239&wNotes=on">cl-PARP↑</a>,
<a href="tbResList.php?qv=61&wNotes=on&word=HSP">HSP↓</a>
<br>

<!-- ANTIOXIDANT : NRF2, SOD, GSH, CAT, HO-1, GPx, GPX4, -->
- May Lower AntiOxidant defense in Cancer Cells:
<a href="tbResList.php?qv=61&tsv=226&wNotes=on&word=NRF2↓">NRF2↓</a>,
<a href="tbResList.php?qv=61&tsv=137&wNotes=on&word=GSH↓">GSH↓</a>
<a href="tbResList.php?qv=61&tsv=597&wNotes=on">HO1↓</a>


<br>

- May Raise
<a href="tbResList.php?qv=61&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a>
defense in Normal Cells:
<a href="tbResList.php?qv=61&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>,
<a href="tbResList.php?qv=61&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>,
<a href="tbResList.php?qv=61&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>,
<a href="tbResList.php?qv=61&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>,
<a href="tbResList.php?qv=61&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>,
<br>

<!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, -->
- lowers
<a href="tbResList.php?qv=61&tsv=953&wNotes=on&word=Inflam">Inflammation</a> :
<a href="tbResList.php?qv=61&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>,
<a href="tbResList.php?qv=61&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>,
Pro-Inflammatory Cytokines :
<a href="tbResList.php?qv=61&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>,
<a href="tbResList.php?qv=61&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>,
<a href="tbResList.php?qv=61&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>,
<br>



<!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓
inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.-->
- inhibit Growth/Metastases :
<a href="tbResList.php?qv=61&tsv=604&wNotes=on">TumMeta↓</a>,
<a href="tbResList.php?qv=61&tsv=323&wNotes=on">TumCG↓</a>,
<a href="tbResList.php?qv=61&tsv=96&wNotes=on">EMT↓</a>,
<a href="tbResList.php?qv=61&tsv=201&wNotes=on">MMP2↓</a>,
<a href="tbResList.php?qv=61&tsv=203&wNotes=on">MMP9↓</a>,
<a href="tbResList.php?qv=61&tsv=308&wNotes=on">TIMP2</a>,
<a href="tbResList.php?qv=61&tsv=428&wNotes=on">uPA↓</a>,
<a href="tbResList.php?qv=61&tsv=334&wNotes=on">VEGF↓</a>,
<a href="tbResList.php?qv=61&tsv=1284&wNotes=on">ROCK1↓</a>,
<a href="tbResList.php?qv=61&tsv=110&wNotes=on">FAK↓</a>,
<a href="tbResList.php?qv=61&tsv=273&wNotes=on">RhoA↓</a>,
<a href="tbResList.php?qv=61&tsv=214&wNotes=on">NF-κB↓</a>,
<a href="tbResList.php?qv=61&tsv=105&wNotes=on">ERK↓</a>
<br>

<!-- REACTIVATE GENES : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, -->
- reactivate genes thereby inhibiting cancer cell growth :
<a href="tbResList.php?qv=61&tsv=140&wNotes=on">HDAC↓</a>,
<a href="tbResList.php?qv=61&tsv=236&wNotes=on">P53↑</a>,
<a href="tbResList.php?qv=61&wNotes=on&word=HSP">HSP↓</a>,
<br>

<!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ -->
- cause Cell cycle arrest :
<a href="tbResList.php?qv=61&tsv=322&wNotes=on">TumCCA↑</a>,
<a href="tbResList.php?qv=61&tsv=73&wNotes=on">cyclin D1↓</a>,
<a href="tbResList.php?qv=61&tsv=467&wNotes=on">CDK2↓</a>,
<a href="tbResList.php?qv=61&tsv=894&wNotes=on">CDK4↓</a>,
<br>

<!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, -->
- inhibits Migration/Invasion :
<a href="tbResList.php?qv=61&tsv=326&wNotes=on">TumCMig↓</a>,
<a href="tbResList.php?qv=61&tsv=324&wNotes=on">TumCI↓</a>,
<a href="tbResList.php?qv=61&tsv=110&wNotes=on">FAK↓</a>,
<a href="tbResList.php?qv=61&tsv=105&wNotes=on">ERK↓</a>,
<a href="tbResList.php?qv=61&tsv=96&wNotes=on">EMT↓</a>,
<a href="tbResList.php?qv=61&tsv=1117&wNotes=on">TOP1↓</a>,
<a href="tbResList.php?qv=61&tsv=657&wNotes=on">TET1↓</a>,
<br>

<!-- GLYCOLYSIS : ATP↓, HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓, Glucose↓, GlucoseCon↓, lactateProd, OXPHOS -->
- inhibits
<a href="tbResList.php?qv=61&tsv=129&wNotes=on">glycolysis</a>
and
<a href="tbResList.php?qv=61&tsv=21&wNotes=on&word=ATP↓">ATP depletion</a> :
<a href="tbResList.php?qv=61&tsv=143&wNotes=on">HIF-1α↓</a>,
<a href="tbResList.php?qv=61&tsv=35&wNotes=on">cMyc↓</a>,
<a href="tbResList.php?qv=61&tsv=566&wNotes=on&word=GLUT">GLUT1↓</a>,
<a href="tbResList.php?qv=61&tsv=906&wNotes=on">LDH↓</a>,
<a href="tbResList.php?qv=61&tsv=773&wNotes=on">HK2↓</a>,
<a href="tbResList.php?qv=61&wNotes=on&word=PDK">PDKs↓</a>,
<a href="tbResList.php?qv=61&tsv=773&wNotes=on">HK2↓</a>,
<a href="tbResList.php?qv=61&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=61&tsv=623&wNotes=on">GlucoseCon↓</a>
<br>


<!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)-->
- inhibits
<a href="tbResList.php?qv=61&tsv=447&wNotes=on">angiogenesis↓</a> :
<a href="tbResList.php?qv=61&tsv=334&wNotes=on">VEGF↓</a>,
<a href="tbResList.php?qv=61&tsv=143&wNotes=on">HIF-1α↓</a>,
<a href="tbResList.php?qv=61&wNotes=on&word=NOTCH">Notch↓</a>,
<a href="tbResList.php?qv=61&tsv=361&wNotes=on">PDGF↓</a>,
<a href="tbResList.php?qv=61&tsv=94&wNotes=on&word=EGFR↓">EGFR↓</a>,
<br>


<!-- OTHERS : -->
- Others: <a href="tbResList.php?qv=61&tsv=252&wNotes=on">PI3K↓</a>,
<a href="tbResList.php?qv=61&tsv=4&wNotes=on">AKT↓</a>,
<a href="tbResList.php?qv=61&wNotes=on&word=STAT">STAT↓</a>,
<a href="tbResList.php?qv=61&tsv=377&wNotes=on">Wnt↓</a>,
<a href="tbResList.php?qv=61&tsv=9&wNotes=on">AMPK↓</a>,
<a href="tbResList.php?qv=61&tsv=105&wNotes=on">ERK↓</a>,
<a href="tbResList.php?qv=61&tsv=168&wNotes=on">JNK</a>,
<a href="tbResList.php?qv=61&tsv=825&wNotes=on">TrxR</a>,
<br>


<!-- SYNERGIES : -->
- Synergies:
<a href="tbResList.php?qv=61&tsv=1106&wNotes=on">chemo-sensitization</a>,
<a href="tbResList.php?qv=61&tsv=1171&wNotes=on">chemoProtective</a>,
<a href="tbResList.php?qv=61&tsv=1107&wNotes=on">RadioSensitizer</a>,
<a href="tbResList.php?qv=61&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>,
<a href="tbResList.php?qv=61&tsv=1105&wNotes=on">Neuroprotective</a>,
<a href="tbResList.php?qv=61&tsv=557&wNotes=on">Cognitive</a>,
<a href="tbResList.php?qv=61&tsv=1175&wNotes=on">Renoprotection</a>,
<a href="tbResList.php?qv=61&tsv=1179&wNotes=on">Hepatoprotective</a>,
<a href="tbResList.php?&qv=61&tsv=1188&wNotes=on">CardioProtective</a>,

<br>
<br>
<!-- SELECTIVE: -->
- Selectivity:
<a href="tbResList.php?qv=61&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a>
<br>
<br>



<h3>Chrysin Mechanistic Profile</h3>
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer Cells</th>
<th>Normal Cells</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
<tr>
<td>1</td>
<td>PI3K AKT survival signaling</td>
<td>PI3K↓; AKT phosphorylation↓; survival signaling↓</td>
<td>↔</td>
<td>R, G</td>
<td>Growth and survival suppression</td>
<td>Central hub mechanism reported across multiple tumor models; also supports chemosensitization.</td>
</tr>
<tr>
<td>2</td>
<td>Mitochondrial apoptosis</td>
<td>MMP↓; Bax↑; Bcl-2↓; cytochrome c↑; caspase-9/3↑</td>
<td>↔ or lower sensitivity</td>
<td>R, G</td>
<td>Intrinsic apoptosis execution</td>
<td>One of the most consistent anticancer endpoints, usually downstream of stress and survival-pathway suppression.</td>
</tr>
<tr>
<td>3</td>
<td>Mitochondrial ROS stress</td>
<td>ROS↑ (context-dependent); oxidative stress↑; lipid peroxidation↑</td>
<td>ROS↓ or antioxidant protection (context-dependent)</td>
<td>P, R, G</td>
<td>Stress amplification</td>
<td>Direction is dose- and model-dependent; cancer models often show pro-oxidant stress, while normal injury models may show antioxidant behavior.</td>
</tr>
<tr>
<td>4</td>
<td>ER stress and UPR</td>
<td>ER stress↑; GRP78↑; UPR↑; autophagy or apoptosis↑</td>
<td>↔</td>
<td>R, G</td>
<td>Stress-to-death coupling</td>
<td>Important in several chrysin cancer models and in some drug-combination effects.</td>
</tr>
<tr>
<td>5</td>
<td>NF-κB inflammatory transcription</td>
<td>NF-κB↓; COX-2↓; IL-6↓; TNF-α↓</td>
<td>Inflammatory injury signaling↓</td>
<td>R, G</td>
<td>Anti-inflammatory and anti-survival signaling</td>
<td>May contribute to reduced proliferation, invasion, and cytokine-driven tumor support.</td>
</tr>
<tr>
<td>6</td>
<td>Invasion EMT and MMPs</td>
<td>EMT↓; MMP-2↓; MMP-9↓; uPA↓; migration↓; invasion↓</td>
<td>↔</td>
<td>G</td>
<td>Anti-invasive phenotype</td>
<td>Mechanistically relevant for metastasis models but generally later and context-dependent.</td>
</tr>
<tr>
<td>7</td>
<td>Angiogenesis and HIF-1α VEGF signaling</td>
<td>HIF-1α↓; VEGF↓; angiogenic output↓</td>
<td>↔</td>
<td>G</td>
<td>Anti-angiogenic support</td>
<td>Reported in preclinical models; may overlap with oxidative stress and DNA damage response pathways.</td>
</tr>
<tr>
<td>8</td>
<td>Glycolysis and metabolic stress</td>
<td>GLUT1↓; HK2↓; LDH↓; PDK1↓; lactate production↓; ATP↓</td>
<td>↔</td>
<td>G</td>
<td>Metabolic suppression</td>
<td>Relevant but less central than apoptosis and survival signaling; strongest interpretation is model-dependent.</td>
</tr>
<tr>
<td>9</td>
<td>NRF2 antioxidant axis</td>
<td>NRF2↓ or antioxidant defense↓ (model-dependent)</td>
<td>NRF2↑; SOD↑; GSH↑; catalase↑ (context-dependent)</td>
<td>R, G</td>
<td>Context-dependent redox selectivity</td>
<td>Potentially useful but also interpret carefully because NRF2 activation can be protective in normal cells and sometimes undesirable in cancer cells.</td>
</tr>
<tr>
<td>10</td>
<td>Chemosensitization and radiosensitization</td>
<td>Drug-induced toxicity↑; apoptosis↑; resistance signaling↓</td>
<td>Chemoprotection reported in some injury models</td>
<td>G</td>
<td>Adjunct sensitization</td>
<td>Promising preclinical adjunct signal, but not clinically established.</td>
</tr>
<tr>
<td>11</td>
<td>Clinical Translation Constraint</td>
<td>Systemic exposure low after native oral dosing</td>
<td>Dose and formulation constraints</td>
<td>G</td>
<td>Translation limitation</td>
<td>Very poor oral bioavailability is the dominant practical constraint; formulation or local GI targeting is likely required.</td>
</tr>
</table>

<p><b>Time-Scale Flag (TSF):</b> P / R / G</p>
<ul>
<li><b>P</b>: 0–30 min (primary/physical–chemical effects; rapid signaling / phosphorylation shifts)</li>
<li><b>R</b>: 30 min–3 hr (acute stress-response and redox signaling)</li>
<li><b>G</b>: &gt;3 hr (gene-regulatory adaptation and phenotype-level outcomes)</li>
</ul>



Pathway results for Effect on Cancer / Diseased Cells

NA, unassigned ⓘ

CBR1↓, 1,   SALL4↓, 1,  

Redox & Oxidative Stress ⓘ

Catalase↓, 1,   Fenton↑, 1,   GSH↓, 6,   H2O2↑, 1,   HO-1↓, 3,   lipid-P↑, 3,   MDA↑, 1,   NRF2↓, 6,   ROS↑, 18,   ROS↓, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

ADP:ATP↑, 2,   mt-ATP↓, 1,   ATP↓, 1,   BOK↑, 1,   MMP↓, 9,   MMP↑, 1,   MPT↑, 2,   mtDam↑, 1,   XIAP↓, 4,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   ALAT↓, 2,   AMPK↑, 3,   cMyc↓, 2,   glucose↓, 1,   GlucoseCon↓, 3,   Glycolysis↓, 4,   HK2↓, 6,   lactateProd↓, 3,   LDH↓, 1,   LDL↓, 1,   NADPH↓, 1,   PDK1↓, 3,   PDK3↑, 1,   PPARα↓, 1,  

Cell Death ⓘ

p‑Akt↓, 4,   p‑Akt↑, 1,   Akt↓, 10,   APAF1↑, 1,   Apoptosis↑, 16,   Apoptosis↓, 1,   BAD↓, 1,   Bak↑, 1,   BAX↑, 5,   Bax:Bcl2↑, 1,   Bcl-2↓, 2,   Bcl-xL↓, 1,   BID↑, 1,   Casp↑, 2,   Casp3↑, 14,   Casp7↑, 2,   cl‑Casp7↑, 1,   Casp8↑, 2,   Casp9↑, 8,   Cyt‑c↑, 6,   DR5↑, 1,   FADD↑, 1,   Fas↑, 1,   FasL↑, 1,   hTERT/TERT↓, 6,   iNOS↓, 1,   JNK↑, 2,   JNK↓, 1,   MAPK↑, 3,   MAPK↓, 1,   Mcl-1↓, 2,   NAIP↓, 1,   p27↑, 1,   p38↑, 3,   Proteasome↓, 1,   PUMA↑, 1,   survivin↓, 1,   TRAIL↑, 1,   TumCD↑, 3,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 2,   p‑p70S6↑, 1,   p70S6↓, 1,  

Transcription & Epigenetics ⓘ

p‑cJun↓, 1,   PhotoS↑, 1,   tumCV↓, 6,  

Protein Folding & ER Stress ⓘ

eIF2α↑, 3,   p‑eIF2α↑, 2,   ER Stress↑, 7,   GRP78/BiP↑, 3,   GRP78/BiP↝, 1,   PERK↑, 3,   UPR↑, 6,   XBP-1↓, 1,   XBP-1↝, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 6,   P53↑, 3,   PARP↑, 1,   cl‑PARP↑, 4,   PCNA↓, 5,   TP53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 4,   CDK4↓, 3,   CycB/CCNB1↓, 2,   cycD1/CCND1↓, 7,   cycE1↓, 1,   P21↑, 1,   TumCCA↑, 13,  

Proliferation, Differentiation & Cell State ⓘ

AR-V7?, 1,   p‑cFos↓, 1,   Diff↑, 1,   EMT↓, 5,   ERK↓, 3,   ERK↑, 1,   p‑ERK↑, 1,   GSK‐3β↑, 1,   HDAC↓, 3,   HDAC8↓, 3,   Let-7↑, 1,   mTOR↓, 4,   NOTCH↑, 1,   NOTCH1↑, 4,   PI3K↑, 2,   PI3K↓, 4,   SCF↓, 2,   SHP1↑, 1,   STAT3↑, 1,   STAT3↓, 3,   p‑STAT3↓, 3,   p‑STAT3↑, 1,   TOP1↓, 2,   TumCG↓, 5,   Wnt↓, 1,  

Migration ⓘ

AP-1↓, 1,   Ca+2↑, 5,   Ca+2↓, 1,   CDKN1C↑, 1,   CLDN1↓, 3,   E-cadherin↑, 4,   FAK↓, 2,   p‑FAK↓, 1,   Fibronectin↓, 1,   Ki-67↓, 2,   MMP-10↓, 2,   MMP2↓, 4,   MMP9↑, 1,   MMP9↓, 5,   N-cadherin↓, 1,   PDGF↓, 1,   Rho↓, 1,   ROCK1↓, 1,   Slug↓, 2,   Snail↓, 2,   TET1↑, 5,   TIMP1↑, 1,   TIMP2↑, 1,   TumCI↓, 7,   TumCMig↓, 3,   TumCP↓, 9,   TumMeta↓, 5,   TumMeta↑, 1,   Twist↓, 3,   uPA↓, 1,   Vim↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 11,   ATF4↑, 2,   EGFR↓, 1,   Hif1a↓, 5,   VEGF↓, 7,  

Barriers & Transport ⓘ

BBB↑, 1,   GLUT1↓, 1,   MRP↓, 1,   OATPs↓, 2,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   COX2↓, 6,   COX2↑, 1,   IL10↓, 1,   IL1β↓, 3,   IL2↑, 1,   IL6↓, 2,   Inflam↓, 3,   M2 MC↑, 1,   NF-kB↓, 6,   NF-kB↑, 1,   PD-L1↓, 2,   PGE2↓, 2,   TLR4↓, 2,   TNF-α↑, 1,   TNF-α↓, 3,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CYP19?, 1,   CYP19↓, 1,  

Drug Metabolism & Resistance ⓘ

ABCG2↓, 1,   BioAv↓, 4,   BioAv↑, 8,   BioEnh↝, 1,   ChemoSen↑, 13,   CYP2C9↓, 1,   Dose↝, 3,   eff↑, 28,   Half-Life↓, 2,   Half-Life↑, 1,   MDR1↓, 1,   RadioS↑, 4,   selectivity↑, 7,  

Clinical Biomarkers ⓘ

ALAT↓, 2,   ALP↓, 1,   AR↓, 1,   EGFR↓, 1,   HER2/EBBR2↓, 2,   hTERT/TERT↓, 6,   IL6↓, 2,   Ki-67↓, 2,   LDH↓, 1,   PD-L1↓, 2,   TP53↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   cardioP↑, 1,   chemoP↑, 2,   chemoPv↑, 3,   neuroP↑, 2,   OS↑, 1,   RenoP↑, 1,   TumVol↓, 2,   TumW↓, 1,   Weight∅, 2,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 225

Pathway results for Effect on Normal Cells

NA, unassigned ⓘ

AntiArt↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx↑, 6,   Catalase↑, 5,   Catalase↓, 1,   GPx↑, 3,   GPx↓, 1,   GSH↑, 4,   GSR↑, 1,   GSTs↑, 2,   HDL↑, 1,   HO-1↑, 3,   lipid-P↓, 4,   MDA↓, 3,   NOX4↓, 1,   NRF2↑, 3,   NRF2↓, 1,   ROS↓, 15,   ROS∅, 1,   SOD↑, 6,   TBARS↓, 1,   VitC↑, 1,  

Core Metabolism/Glycolysis ⓘ

CREB↑, 1,   GAPDH↑, 1,   lipidLev↓, 2,   NADPH↑, 1,   PPARα↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 1,   Apoptosis↓, 2,   BAX↓, 1,   Bcl-2↑, 1,   Casp3↓, 2,   Casp9↓, 1,   Cyt‑c↓, 1,   iNOS↓, 2,   JNK↓, 1,   MAPK↓, 1,   MAPK↑, 1,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 2,   P53↑, 1,   PARP↓, 1,   PCNA↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,   HDAC↓, 1,   PI3K↓, 1,   PTEN↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 6,   COX2∅, 1,   IFN-γ↓, 1,   IL17↓, 1,   IL1β↓, 2,   IL2↓, 1,   Inflam↓, 9,   NF-kB↓, 6,   PGE2↓, 1,   TNF-α↓, 3,  

Synaptic & Neurotransmission ⓘ

5HT↑, 1,   AChE↓, 1,   BDNF↑, 2,   GABA↑, 1,   TrkB↑, 1,  

Protein Aggregation ⓘ

AGEs↓, 1,   Aβ↓, 1,  

Hormonal & Nuclear Receptors ⓘ

GR↑, 1,   GR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 7,   BioAv↑, 3,   Dose↝, 1,   eff↓, 1,   eff↑, 2,   P450↓, 1,  

Clinical Biomarkers ⓘ

AST↓, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cardioP↑, 5,   cardioP⇅, 1,   chemoPv↑, 3,   cognitive↑, 2,   hepatoP↑, 6,   memory↑, 4,   neuroP↑, 6,   neuroP↓, 1,   RenoP↑, 3,   toxicity↓, 2,   toxicity↝, 2,  
Total Targets: 87

Research papers

Year Title Authors PMID Link Flag
2026Chrysin and its nanoformulations in cancer therapy: A systematic review of their radiosensitizing, phototherapy-enhancing potentialsMojtaba Saedi Marghmaleki—https://herbmedpharmacol.com/PDF/jhp-15-175.pdf0
2025Anticancer Activity of Ether Derivatives of ChrysinArkadiusz Sokal —https://www.mdpi.com/1420-3049/30/4/9600
2025Network pharmacology unveils the intricate molecular landscape of Chrysin in breast cancer therapeuticsJianping Ma—https://link.springer.com/article/10.1007/s12672-025-01951-30
2025Synergistic anticancer effects of Chrysin and trastuzumab in HER2-Positive breast cancer cellsSevda Jafari—https://www.nature.com/articles/s41598-025-25098-x0
2025Chrysin as a Multifunctional Therapeutic Flavonoid: Emerging Insights in Pathogenesis Management: A Narrative ReviewArshad Husain Rahmani—https://www.mdpi.com/1422-0067/27/1/720
2025Comparative Pharmacokinetics and Safety of a Micellar Chrysin–Quercetin–Rutin Formulation: A Randomized Crossover TrialAfoke Ibi—https://www.mdpi.com/2076-3921/14/11/13130
2025Chrysin modulates the BDNF/TrkB/AKT/Creb neuroplasticity signaling pathway: Acting in the improvement of cognitive flexibility and declarative, working and aversive memory deficits caused by hypothyroidism in C57BL/6 female miceVandreza Cardoso Bortolotto—https://www.sciencedirect.com/science/article/abs/pii/S03064522240073950
2025Chrysin: A Comprehensive Review of Its Pharmacological Properties and Therapeutic PotentialMagdalena KurkiewiczPMC12389306https://pmc.ncbi.nlm.nih.gov/articles/PMC12389306/0
2024Chrysin Inhibits TAMs-Mediated Autophagy Activation via CDK1/ULK1 Pathway and Reverses TAMs-Mediated Growth-Promoting Effects in Non-Small Cell Lung CancerXinglinzi Tang —https://www.mdpi.com/1424-8247/17/4/5150
2024Chrysin targets aberrant molecular signatures and pathways in carcinogenesis (Review)Ritu Raina—https://www.spandidos-publications.com/10.3892/wasj.2024.2600
2023Chrysin a promising anticancer agent: recent perspectivesMuhammad Shahbaz—https://www.tandfonline.com/doi/full/10.1080/10942912.2023.2246678#abstract0
2022Anti-cancer Activity of Chrysin in Cancer Therapy: a Systematic ReviewNader SalariPMC9845454https://pmc.ncbi.nlm.nih.gov/articles/PMC9845454/0
2022Fabrication of phenyl boronic acid modified pH-responsive zinc oxide nanoparticles as targeted delivery of chrysin on human A549 cellsSushweta MahalanobishPMC9301599https://pmc.ncbi.nlm.nih.gov/articles/PMC9301599/0
2022Evidence-based mechanistic role of chrysin towards protection of cardiac hypertrophy and fibrosis in ratsSonali Meshram—https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/evidencebased-mechanistic-role-of-chrysin-towards-protection-of-cardiac-hypertrophy-and-fibrosis-in-rats/F981072347E66679932F162E177229890
2021Developing nutritional component chrysin as a therapeutic agent: Bioavailability and pharmacokinetics consideration, and ADME mechanismsSong Gao—https://www.sciencedirect.com/science/article/pii/S07533322210086350
2021Chrysin inhibits propagation of HeLa cells by attenuating cell survival and inducing apoptotic pathwaysR Raina33755959https://pubmed.ncbi.nlm.nih.gov/33755959/0
2021Emerging cellular and molecular mechanisms underlying anticancer indications of chrysinMarjan Talebi—https://cancerci.biomedcentral.com/articles/10.1186/s12935-021-01906-y0
2021Chrysin inhibits hepatocellular carcinoma progression through suppressing programmed death ligand 1 expressionWeihao Rong34923234https://pubmed.ncbi.nlm.nih.gov/34923234/0
2021An updated review on the versatile role of chrysin in neurological diseases: Chemistry, pharmacology, and drug delivery approachesMarjan Talebi—https://www.sciencedirect.com/science/article/pii/S07533322210068800
2020Chrysin Induced Cell Apoptosis and Inhibited Invasion Through Regulation of TET1 Expression in Gastric Cancer CellsXiaowei ZhongPMC7182457https://pmc.ncbi.nlm.nih.gov/articles/PMC7182457/0
2020Effects of Chrysin and Its Major Conjugated Metabolites Chrysin-7-Sulfate and Chrysin-7-Glucuronide on Cytochrome P450 Enzymes and on OATP, P-gp, BCRP, and MRP2 TransportersVioletta Mohos—https://www.sciencedirect.com/science/article/abs/pii/S00909556240786190
2020Chrysin serves as a novel inhibitor of DGKα/FAK interaction to suppress the malignancy of esophageal squamous cell carcinoma (ESCC)Jie ChenPMC7838054https://pmc.ncbi.nlm.nih.gov/articles/PMC7838054/0
2020Potentiating activities of chrysin in the therapeutic efficacy of 5-fluorouracil in gastric cancer cellsSunyi LeePMC7681229https://pmc.ncbi.nlm.nih.gov/articles/PMC7681229/0
2020Inhibition of Hypoxia-Inducible Factor-1α and Vascular Endothelial Growth Factor by Chrysin in a Rat Model of Choroidal NeovascularizationJi Hun SongPMC7215732https://pmc.ncbi.nlm.nih.gov/articles/PMC7215732/0
2020Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future PerspectivesEbrahim Rahmani MoghadamPMC7600196https://pmc.ncbi.nlm.nih.gov/articles/PMC7600196/0
2019Chrysin enhances anticancer drug-induced toxicity mediated by the reduction of claudin-1 and 11 expression in a spheroid culture model of lung squamous cell carcinoma cellsRyohei MaruhashiPMC6760125https://pmc.ncbi.nlm.nih.gov/articles/PMC6760125/0
2019Gamma-Irradiated Chrysin Improves Anticancer Activity in HT-29 Colon Cancer Cells Through Mitochondria-Related PathwayHa-Yeon Song31158040https://pubmed.ncbi.nlm.nih.gov/31158040/0
2019Chrysin: Pharmacological and therapeutic propertiesSaima Naz—https://www.sciencedirect.com/science/article/abs/pii/S00243205193072460
2018Chrysin attenuates progression of ovarian cancer cells by regulating signaling cascades and mitochondrial dysfunctionWhasun Lim—https://pubmed.ncbi.nlm.nih.gov/28816359/0
2018Synergistic Growth Inhibitory Effects of Chrysin and Metformin Combination on Breast Cancer Cells through hTERT and Cyclin D1 SuppressionSara RasouliPMC6031784https://pmc.ncbi.nlm.nih.gov/articles/PMC6031784/0
2018Chrysin suppresses proliferation, migration, and invasion in glioblastoma cell lines via mediating the ERK/Nrf2 signaling pathwayJuan WangPMC5892952https://pmc.ncbi.nlm.nih.gov/articles/PMC5892952/0
2018Chrysin: Sources, beneficial pharmacological activities, and molecular mechanism of actionRenuka Mani—https://www.sciencedirect.com/science/article/abs/pii/S00319422173032170
2017Chrysin as an Anti-Cancer Agent Exerts Selective Toxicity by Directly Inhibiting Mitochondrial Complex II and V in CLL B-lymphocytesAhmad Salimi28301251https://pubmed.ncbi.nlm.nih.gov/28301251/0
2017Chrysin inhibited tumor glycolysis and induced apoptosis in hepatocellular carcinoma by targeting hexokinase-2Dong XuPMC5359903https://pmc.ncbi.nlm.nih.gov/articles/PMC5359903/0
2017Chrysin induces death of prostate cancer cells by inducing ROS and ER stressSoomin Ryu28213961https://pubmed.ncbi.nlm.nih.gov/28213961/0
2016Anticancer Properties of Chrysin on Colon Cancer Cells, In vitro and In vivo with Modulation of Caspase-3, -9, Bax and Sall4Maliheh BahadoriPMC5492241https://pmc.ncbi.nlm.nih.gov/articles/PMC5492241/0
2016Chrysin induces cell apoptosis in human uveal melanoma cells via intrinsic apoptosisChunyan XuePMC5228444https://pmc.ncbi.nlm.nih.gov/articles/PMC5228444/0
2016Chemopreventive effect of chrysin, a dietary flavone against benzo(a)pyrene induced lung carcinogenesis in Swiss albino miceEshvendar Reddy Kasala26922533https://pubmed.ncbi.nlm.nih.gov/26922533/0
2015Combination of chrysin and cisplatin promotes the apoptosis of Hep G2 cells by up-regulating p53Xin Li25770930https://pubmed.ncbi.nlm.nih.gov/25770930/0
2015Chrysin Inhibits Tumor Promoter-Induced MMP-9 Expression by Blocking AP-1 via Suppression of ERK and JNK Pathways in Gastric Cancer CellsYong XiaPMC4398353https://pmc.ncbi.nlm.nih.gov/articles/PMC4398353/0
2015Selenium-containing chrysin and quercetin derivatives: attractive scaffolds for cancer therapyInês L Martins25906385https://pubmed.ncbi.nlm.nih.gov/25906385/0
2015Chemopreventive and therapeutic potential of chrysin in cancer: mechanistic perspectivesEshvendar Reddy Kasala25596314https://pubmed.ncbi.nlm.nih.gov/25596314/0
2014Chrysin in PI3K/AKT and other apoptosis signalling pathways, and its effect on HeLa cells.Khoo Boon Yin—https://www.researchgate.net/publication/262144098_Chrysin_in_PI3KAKT_and_other_apoptosis_signalling_pathways_and_its_effect_on_HeLa_cells?0
2014Chrysin Activates Notch1 Signaling and Suppresses Tumor Growth of Anaplastic Thyroid Carcinoma In vitro and In vivoXiao-Min YuPMC3528831https://pmc.ncbi.nlm.nih.gov/articles/PMC3528831/0
2014Chrysin inhibits metastatic potential of human triple-negative breast cancer cells by modulating matrix metalloproteinase-10, epithelial to mesenchymal transition, and PI3K/Akt signaling pathwayBing Yang24122885https://pubmed.ncbi.nlm.nih.gov/24122885/0
2013Chrysin enhances sensitivity of BEL-7402/ADM cells to doxorubicin by suppressing PI3K/Akt/Nrf2 and ERK/Nrf2 pathwayAi-Mei Gao23994249https://pubmed.ncbi.nlm.nih.gov/23994249/0
2013A flavonoid chrysin suppresses hypoxic survival and metastatic growth of mouse breast cancer cellsKriengsak Lirdprapamongkol23969634https://pubmed.ncbi.nlm.nih.gov/23969634/0
2013Chrysin suppresses renal carcinogenesis via amelioration of hyperproliferation, oxidative stress and inflammation: plausible role of NF-κBMuneeb U Rehman23194824https://pubmed.ncbi.nlm.nih.gov/23194824/0
2013A Chrysin Derivative Suppresses Skin Cancer Growth by Inhibiting Cyclin-dependent KinasesHaidan LiuPMC3764797https://pmc.ncbi.nlm.nih.gov/articles/PMC3764797/0
2012AMP-activated protein kinase (AMPK) activation is involved in chrysin-induced growth inhibition and apoptosis in cultured A549 lung cancer cellsJun-jie Shao22659738https://pubmed.ncbi.nlm.nih.gov/22659738/0
2012Chrysin protects against cisplatin-induced colon. toxicity via amelioration of oxidative stress and apoptosis: Probable role of p38MAPK and p53Rehan Khan—https://www.sciencedirect.com/science/article/abs/pii/S0041008X110044920
2012Chrysin: a histone deacetylase 8 inhibitor with anticancer activity and a suitable candidate for the standardization of Chinese propolisLi-Ping Sun23134323https://pubmed.ncbi.nlm.nih.gov/23134323/0
2011The anticancer flavonoid chrysin induces the unfolded protein response in hepatoma cellsXiangming SunPMC3822950https://pmc.ncbi.nlm.nih.gov/articles/PMC3822950/0
20108-bromo-7-methoxychrysin-induced apoptosis of hepatocellular carcinoma cells involves ROS and JNKXiao-Hong YangPMC2904884https://pmc.ncbi.nlm.nih.gov/articles/PMC2904884/0
2010Apoptotic Effects of Chrysin in Human Cancer Cell LinesBoon Yin KhooPMC2885101https://pmc.ncbi.nlm.nih.gov/articles/PMC2885101/0
2007Chrysin inhibits expression of hypoxia-inducible factor-1alpha through reducing hypoxia-inducible factor-1alpha stability and inhibiting its protein synthesisBeibei Fu17237281https://pubmed.ncbi.nlm.nih.gov/17237281/0
2001Disposition and metabolism of the flavonoid chrysin in normal volunteersT WallePMC2014445https://pmc.ncbi.nlm.nih.gov/articles/PMC2014445/0
2014Flavonoid-induced glutathione depletion: Potential implications for cancer treatmentRemy KachadourianPMC3983951https://pmc.ncbi.nlm.nih.gov/articles/PMC3983951/0
2022An update of Nrf2 activators and inhibitors in cancer prevention/promotionFarhad PouremamaliPMC9245222https://pmc.ncbi.nlm.nih.gov/articles/PMC9245222/0
2006Luteolin and chrysin differentially inhibit cyclooxygenase-2 expression and scavenge reactive oxygen species but similarly inhibit prostaglandin-E2 formation in RAW 264.7 cellsGabriel K Harris16702314https://pubmed.ncbi.nlm.nih.gov/16702314/0