Database Query Results : Chrysin, , hepatoP

CHr, Chrysin: Click to Expand ⟱

Features:

Chrysin is found in passion flower and honey. It is a flavonoid.
-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.
Chrysin is widely summarized as modulating PI3K/Akt and MAPK pathways in cancer.

-Note half-life 2 hrs, BioAv very poor often <1%
Pathways:
Graphical Pathways

- may induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- May Lower AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓ HO1↓
- May Raise AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMP2↓, MMP9↓, TIMP2, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, P53↑, HSP↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, cMyc↓, GLUT1↓, LDH↓, HK2↓, PDKs↓, HK2↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, PDGF↓, EGFR↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, AMPK↓, ERK↓, JNK, TrxR,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	PI3K → AKT (± mTOR) survival axis	↓ PI3K/AKT (often ↓ p-AKT; downstream growth signals ↓)	↔	R, G	Growth/survival suppression	Frequently reported hub effect; contributes to reduced proliferation and sensitization to stress/apoptosis programs.
2	Intrinsic apoptosis (p53/Bcl-2 family → caspase-9/3)	↑ p53 axis (context); Bax↑/Bcl-2↓; ↑ caspase-9/3; apoptosis ↑	↔ (generally less activation)	G	Apoptosis execution	Common endpoint across many tumor models; often downstream of survival-pathway suppression and stress signaling.
3	ER stress / UPR (PERK and related arms)	ER stress ↑; UPR activation ↑	↔	R, G	Stress-to-death coupling	ER stress has been directly shown in chrysin-treated cancer cells and can couple to apoptosis.
4	JAK / STAT3 signaling	↓ STAT3 signaling (context)	↔	R, G	Anti-survival transcription	STAT3 inhibition is reported in cancer models and often aligns with reduced proliferation and increased apoptosis.
5	ROS / oxidative stress (context-dependent)	ROS modulation (often ↑ mitochondrial ROS in tumor models)	↔ / antioxidant behavior in some contexts	P, R, G	Stress amplifier (variable)	Direction depends on dose/model; avoid absolute “ROS always ↑/↓”. Oxidative stress + DDR has been linked to anti-angiogenic effects in vivo in melanoma models.
6	MAPK re-wiring (ERK / JNK / p38)	MAPK shifts; JNK/p38 often stress-activated; ERK variable	↔	P, R, G	Signal reprogramming	MAPK effects differ by cell line; chrysin can suppress JNK/ERK signaling to reduce MMP-9 in some models.
7	Cell-cycle arrest / proliferation control	Cell-cycle arrest ↑; proliferation ↓	↔	G	Cytostasis	Often observed as later phenotype-level outcomes, downstream of signaling changes.
8	Invasion / metastasis (MMP-9; EMT programs)	MMP-9 ↓; migration/invasion ↓ (context)	↔	G	Anti-invasive phenotype	Chrysin can reduce MMP-9 expression via AP-1 suppression and MAPK pathway effects in certain cancer models.
9	Angiogenesis (VEGF/angiogenic outputs)	Angiogenesis outputs ↓ (context)	↔	G	Anti-angiogenic support	In melanoma models, chrysin has been associated with angiogenesis regression linked to oxidative stress and DNA damage response.
10	Bioavailability constraint (oral PK limitation)	Systemic exposure often low without formulation	—	—	Translation constraint	Native chrysin oral bioavailability is extremely low due to poor solubility and extensive glucuronidation/sulfation with efflux; formulation strategies are commonly required for systemic effects.

Time-Scale Flag (TSF): P / R / G

P: 0–30 min (primary/physical–chemical effects; rapid signaling / phosphorylation shifts)
R: 30 min–3 hr (acute stress-response and redox signaling)
G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)

hepatoP, L,hepatoprotective: Click to Expand ⟱

Source:

Type:

Hepatoprotective is the ability of a chemical substance to prevent damage to the liver.

Grapefruit:
-hepatoprotective potential has emerged from the study of naringenin and naringin.
Blueberries/cranberries:
-proanthocyanidins
Grape:
Nopal (Cactus pear) and tuna (Cactus pear fruit) “Opuntia ficus-indica”:
Chamomile (Matricaria chamomilla or Chamomilla recutita):
Silymarin (Silybum marianum):
Blue green algae spirulina :
Propolis (bee glue):

POLYSACCHARIDES
β-glucans

Scientific Papers found: Click to Expand⟱

2790-

CHr,

Chrysin: Pharmacological and therapeutic properties

Review,

Var,

*hepatoP↑, graphical abstract
*neuroP↓,
*ROS↓,
*cardioP↑,
*Inflam↓,
eff↑, suppression of hTERT and cyclin D1 gene expression in T47D breast cancer cell lines is due to the combined effect of metformin and chrysin
hTERT/TERT↓,
cycD1/CCND1↓,
MMP9↓, nanoparticle-based chrysin in C57B16 mice bearing B16F10 melanoma tumors was markedly presented reductions in the levels of MMP-9, MMP-2, and TERT genes, whereas it enhanced TIMP-2 andTIMP-1 genes expression
MMP2↓,
TIMP1↑,
TIMP2↑,
BioAv↑, nano-encapsulation of chrysin and curcumin improved the delivery of these phytochemicals that significantly inhibited the growth of cancer cells, while it decreased the hTERT gene expression via increased solubility and bioavailability
HK2↓, chrysin treatment restrained tumor growth in HCC xenograft models and significantly reduced HK-2 expression in tumor tissue
ROS↑, showing a significant increase in intracellular reactive oxygen species (ROS), cytotoxicity, mitochondrial membrane potential (MMP) collapse, caspase-3 activation, ADP/ATP ratio, and ultimately apoptosis
MMP↓,
Casp3↑,
ADP:ATP↑,
Apoptosis↑,
ER Stress↑, Likewise, chrysin encouraged endoplasmic reticulum (ER) stress via stimulation of unfolded protein response (UPR
UPR↑,
GRP78/BiP↝, (eIF2Î±), PRKR-like ER kinase (PERK) and 78 kDa glucose-regulated protein (GRP78).
eff↑, silibinin and chrysin synergistically inhibited growth of T47D BCC and downregulated the hTERT and cyclin D1 level
Ca+2↑, Primarily, increased ROS and cytoplasmic Ca 2+ levels alongside induction of cell death and loss of MMP are involved in inhibition of ovarian cancer through chrysin.

2788-

CHr,

Chrysin: Sources, beneficial pharmacological activities, and molecular mechanism of action

Review,

Var,

*neuroP↑, Chrysin mitigates neurotoxicity, neuroinflammation, and oxidative stress.
*Inflam↓,
*ROS↓,
NF-kB↓, Chrysin treatment maintains the antioxidant armory and suppresses the activation of redox-active transcription factor NF-kB
*PCNA↓, Chrysin supplementation downregulated the expression of PCNA, COX-2, and NF-kB
*COX2↓,
ChemoSen↑, Chrysin is effective in attenuating cisplatin-induced expression of both COX-2 and iNOS
Hif1a↓, DU145: Chrysin suppressed the expression of HIF-1a of tumor cells in vitro and inhibited tumor cell-induced angiogenesis in vivo
angioG↓,
*chemoPv↑, Chrysin as an effective chemopreventive agent having the capability to obstruct DEN initiated and Fe-NTA promoted renal cancer in the rat model
PDGF↓, Chrysin functionally suppresses PDGF-induced proliferation and migration in VSMCs
*memory↑, Chrysin is effective in attenuating memory impairment, oxidative stress, acting as an antiaging agent
*RenoP↑, protected the kidney from damage
*PPARα↑, Chrysin significantly inhibits AGE-RAGE mediated oxidative stress and inflammation through PPAR-g activation
*lipidLev↓, Chrysin was able to decrease plasma lipids concentration because of its antioxidant properties
*hepatoP↑, Chrysin shows promising hepatoprotective and antihyperlipidemic effects, which are evidenced by the decreased levels of triglycerides, free fatty acids, total cholesterol, phospholipids, low-density lipoprotein-C, and very low-density lipoprotein
*cardioP⇅, Chrysin significantly ameliorated myocardial damage
*BioAv↓, despite its therapeutic potential, the bioavailability of chrysin and probably other flavonoids in humans is extremely low, mainly due to poor absorption, rapid metabolism, and rapid systemic elimination.

2780-

CHr,

Anti-cancer Activity of Chrysin in Cancer Therapy: a Systematic Review

Review,

Var,

*antiOx↑, antioxidant (13), anti-inflammatory (14), antibacterial (15), anti-hypertensive (16), anti-allergic (17), vasodilator (18),
Inflam↓,
*hepatoP↑, anti-diabetic (19), anti-anxiety (10), anti-viral (20), anti-estrogen (21), liver protective (22), anti-aging (23), anti-seizure (24), and anti-cancer effects (25)
AntiCan↑,
Cyt‑c↑, (1) facilitating the release of cytochrome C from the mitochondria,
Casp3↑, (2) activating caspase-3 and inhibiting the activity of the XIAP molecule,
XIAP↓,
p‑Akt↓, (3) reducing AKT phosphorylation and triggering the PI3K pathway and induction of apoptosis
PI3K↑,
Apoptosis↑,
COX2↓, chrysin interacts weakly with COX-1 binding site whereas displayed a remarkable interaction with COX-2.
FAK↓, ESCC cells: resultant blockage of the FAK/AKT signaling pathways
AMPK↑, A549: activation of AMPK by chrysin contributes to Akt suppression
STAT3↑, 4T1cell: inhibited STAT3 activation
MMP↓, Chrysin induces apoptosis through the intrinsic mitochondrial pathway that disrupts mitochondrial membrane potential (MMP) and increases DNA fragmentation.
DNAdam↑,
BAX↑, produces pro-apoptotic proteins, including Bax and Bak, and activates caspase-9 and caspase-3 in various cancer cells
Bak↑,
Casp9↑,
p38↑, chrysin can inhibit tumor growth by activating P38 MAPK and stopping the cell cycle
MAPK↑,
TumCCA↑,
ChemoSen↑, beneficial in inhibiting chemotherapy resistance of cancer cells
HDAC8↓, chrysin suppresses tumorigenesis by inhibiting histone deacetylase 8 (HDAC8)
Wnt↓, chrysin can attenuate Wnt and NF-κB signaling pathways
NF-kB↓,
angioG↓, chrysin can inhibit angiogenesis and inducing apoptosis in HTh7 cells, 4T1 mice, and MDA-MB-231 cells
BioAv↓, low bioavailability of flavonoids such as chrysin

2781-

CHr,

PBG,

Chrysin a promising anticancer agent: recent perspectives

Review,

Var,

PI3K↓, It can block Phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) and Mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling in different animals against various cancers
Akt↓,
mTOR↓,
MMP9↑, Chrysin strongly suppresses Matrix metalloproteinase-9 (MMP-9), Urokinase plasminogen activator (uPA) and Vascular endothelial growth factor (VEGF), i.e. factors that can cause cancer
uPA↓,
VEGF↓,
AR↓, Chrysin has the ability to suppress the androgen receptor (AR), a protein necessary for prostate cancer development and metastasis
Casp↑, starts the caspase cascade and blocks protein synthesis to kill lung cancer cells
TumMeta↓, Chrysin significantly decreased lung cancer metastasis i
TumCCA↑, Chrysin induces apoptosis and stops colon cancer cells in the G2/M cell cycle phase
angioG↓, Chrysin prevents tumor growth and cancer spread by blocking blood vessel expansion
BioAv↓, Chrysin’s solubility, accessibility and bioavailability may limit its medical use.
*hepatoP↑, As chrysin reduced oxidative stress and lipid peroxidation in rat liver cells exposed to a toxic chemical agent.
*neuroP↑, Protecting the brain against oxidative stress (GPx) may be aided by increasing levels of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx).
*SOD↑,
*GPx↑,
*ROS↓, A decrease in oxidative stress and an increase in antioxidant capacity may result from chrysin’s anti-inflammatory properties
*Inflam↓,
*Catalase↑, Supplementation with chrysin increased the activity of antioxidant enzymes like SOD and catalase and reduced the levels of oxidative stress markers like malondialdehyde (MDA) in the colon tissue of the rats.
*MDA↓, Antioxidant enzyme activity (SOD, CAT) and oxidative stress marker (MDA) levels were both enhanced by chrysin supplementation in mouse liver tissue
ROS↓, reduction of reactive oxygen species (ROS) and oxidative stress markers in the cancer cells further indicated the antioxidant activity of chrysin
BBB↑, After crossing the blood-brain barrier, it has been shown to accumulate there
Half-Life↓, The half-life of chrysin in rats is predicted to be close to 2 hours.
BioAv↑, Taking chrysin with food may increase the effectiveness of the supplement: increased by a factor of 1.8 when taken with a high-fat meal
ROS↑, In contrast to 5-FU/oxaliplatin, chrysin increases the production of reactive oxygen species (ROS), which in turn causes autophagy by stopping Akt and mTOR from doing their jobs
eff↑, mixture of chrysin and cisplatin caused the SCC-25 and CAL-27 cell lines to make more oxygen free radicals. After treatment with chrysin, cisplatin, or both, the amount of reactive oxygen species (ROS) was found to have gone up.
ROS↑, When reactive oxygen species (ROS) and calcium levels in the cytoplasm rise because of chrysin, OC cells die.
ROS↑, chrysin is the cause of death in both types of prostate cancer cells. It does this by depolarizing mitochondrial membrane potential (MMP), making reactive oxygen species (ROS), and starting lipid peroxidation.
lipid-P↑,
ER Stress↑, when chrysin is present in DU145 and PC-3 cells, the expression of a group of proteins that control ER stress goes up
NOTCH1↑, Chrysin increased the production of Notch 1 and hairy/enhancer of split 1 at the protein and mRNA levels, which stopped cells from dividing
NRF2↓, Not only did chrysin stop Nrf2 and the genes it controls from working, but it also caused MCF-7 breast cancer cells to die via apoptosis.
p‑FAK↓, After 48 hours of treatment with chrysin at amounts between 5 and 15 millimoles, p-FAK and RhoA were greatly lowered
Rho↓,
PCNA↓, Lung histology and immunoblotting studies of PCNA, COX-2, and NF-B showed that adding chrysin stopped the production of these proteins and maintained the balance of cells
COX2↓,
NF-kB↓,
PDK1↓, After the chrysin was injected, the genes PDK1, PDK3, and GLUT1 that are involved in glycolysis had less expression
PDK3↑,
GLUT1↓,
Glycolysis↓, chrysin stops glycolysis
mt-ATP↓, chrysin inhibits complex II and ATPases in the mitochondria of cancer cells
Ki-67↓, the amounts of Ki-67, which is a sign of growth, and c-Myc in the tumor tissues went down
cMyc↓,
ROCK1↓, (ROCK1), transgelin 2 (TAGLN2), and FCH and Mu domain containing endocytic adaptor 2 (FCHO2) were much lower.
TOP1↓, DNA topoisomerases and histone deacetylase were inhibited, along with the synthesis of the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and (IL-1 beta), while the activity of protective signaling pathways was increased
TNF-α↓,
IL1β↓,
CycB/CCNB1↓, Chrysin suppressed cyclin B1 and CDK2 production in order to stop cancerous growth.
CDK2↓,
EMT↓, chrysin treatment can also stop EMT
STAT3↓, chrysin block the STAT3 and NF-B pathways, but it also greatly reduced PD-L1 production both in vivo and in vitro.
PD-L1↓,
IL2↑, chrysin increases both the rate of T cell growth and the amount of IL-2

2782-

CHr,

Broad-Spectrum Preclinical Antitumor Activity of Chrysin: Current Trends and Future Perspectives

Review,

Var,

Review,

Stroke,

Review,

Park,

*antiOx↑, antioxidant, anti-inflammatory, hepatoprotective, neuroprotective
*Inflam↓, inhibitory effect of chrysin on inflammation and oxidative stress is also important in Parkinson’s disease
*hepatoP↑,
*neuroP↑,
*BioAv↓, Accumulating data demonstrates that poor absorption, rapid metabolism, and systemic elimination are responsible for poor bioavailability of chrysin in humans that, subsequently, restrict its therapeutic effects
*cardioP↑, cardioprotective [69], lipid-lowering effect [70]
*lipidLev↓,
*RenoP↑, Renoprotective
*TNF-α↓, chrysin reduces levels of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-2 (IL-2).
*IL2↓,
*PI3K↓, induction of the PI3K/Akt signaling pathway by chrysin contributes to a reduction in oxidative stress and inflammation during cerebral I/R injury
*Akt↓,
*ROS↓,
*cognitive↑, Chrysin (25, 50, and 100 mg/kg) improves cognitive capacity, inflammation, and apoptosis to ameliorate traumatic brain injury
eff↑, chrysin and silibinin is beneficial in suppressing breast cancer malignancy via decreasing cancer proliferation
cycD1/CCND1↓, chrysin and silibinin induced cell cycle arrest via down-regulation of cyclin D1 and hTERT
hTERT/TERT↓,
VEGF↓, Administration of chrysin is associated with the disruption of hypoxia-induced VEGF gene expression
p‑STAT3↓, chrysin is capable of reducing STAT3 phosphorylation in hypoxic conditions without affecting the HIF-1α protein level.
TumMeta↓, chrysin is a potent agent in suppressing metastasis and proliferation of breast cancer cells during hypoxic conditions
TumCP↓,
eff↑, combination therapy of breast cancer cells using chrysin and metformin exerts a synergistic effect and is more efficient compared to chrysin alone
eff↑, combination of quercetin and chrysin reduced levels of pro-inflammatory factors, such as IL-1β, Il-6, TNF-α, and IL-10, via NF-κB down-regulation.
IL1β↓,
IL6↓,
NF-kB↓,
ROS↑, after chrysin administration, an increase occurs in levels of ROS that, subsequently, impairs the integrity of the mitochondrial membrane, leading to cytochrome C release and apoptosis induction
MMP↓,
Cyt‑c↑,
Apoptosis↑,
ER Stress↑, in addition to mitochondria, ER can also participate in apoptosis
Ca+2↑, Upon chrysin administration, an increase occurs in levels of ROS and cytoplasmic Ca2+ that mediate apoptosis induction in OC cells
TET1↑, In MKN45 cells, chrysin promotes the expression of TET1
Let-7↑, Chrysin is capable of promoting the expression of miR-9 and Let-7a as onco-suppressor factors in cancer to inhibit the proliferation of GC cells
Twist↓, Down-regulation of NF-κB, and subsequent decrease in Twist/EMT are mediated by chrysin administration, negatively affecting cervical cancer metastasis
EMT↓,
TumCCA↑, nduction of cell cycle arrest and apoptosis via up-regulation of caspase-3, caspase-9, and Bax are mediated by chrysin
Casp3↑,
Casp9↑,
BAX↑,
HK2↓, Chrysin administration (15, 30, and 60 mM) reduces the expression of HK-2 in hepatocellular carcinoma (HCC) cells to impair glucose uptake and lactate production.
GlucoseCon↓,
lactateProd↓,
Glycolysis↓, In addition to glycolysis metabolism impairment, the inhibitory effect of chrysin on HK-2 leads to apoptosis
SHP1↑, upstream modulator of STAT3 known as SHP-1 is up-regulated by chrysin
N-cadherin↓, Furthermore, N-cadherin and E-cadherin are respectively down-regulated and up-regulated upon chrysin administration in inhibiting melanoma invasion
E-cadherin↑,
UPR↑, chrysin substantially diminishes survival by ER stress induction via stimulating UPR, PERK, ATF4, and elF2α
PERK↑,
ATF4↑,
eIF2α↑,
RadioS↑, Irradiation combined with chrysin exerts a synergistic effect
NOTCH1↑, Irradiation combined with chrysin exerts a synergistic effect
NRF2↓, in reducing Nrf2 expression, chrysin down-regulates the expression of ERK and PI3K/Akt pathways—leading to an increase in the efficiency of doxorubicin in chemotherapy
BioAv↑, chrysin at the tumor site by polymeric nanoparticles leads to enhanced anti-tumor activity, due to enhanced cellular uptake
eff↑, Chrysin- and curcumin-loaded nanoparticles significantly promote the expression of TIMP-1 and TIMP-2 to exert a reduction in melanoma invasion

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

AntiCan↑, 1,
Total Targets: 98

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 2, Catalase↑, 1, GPx↑, 1, MDA↓, 1, ROS↓, 4, SOD↑, 1,

Core Metabolism/Glycolysis ⓘ

lipidLev↓, 2, PPARα↑, 1,

Cell Death ⓘ

Akt↓, 1,

DNA Damage & Repair ⓘ

PCNA↓, 1,

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, IL2↓, 1, Inflam↓, 4, TNF-α↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,

Functional Outcomes ⓘ

cardioP↑, 2, cardioP⇅, 1, chemoPv↑, 1, cognitive↑, 1, hepatoP↑, 5, memory↑, 1, neuroP↓, 1, neuroP↑, 3, RenoP↑, 2,
Total Targets: 25

Scientific Paper Hit Count for: hepatoP, L,hepatoprotective

5 Chrysin
1 Propolis -bee glue

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:61  Target#:1179  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Database Query Results : Chrysin, , hepatoP

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

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