Honokiol / RadioS Cancer Research Results

HNK, Honokiol: Click to Expand ⟱

Features:

Honokiol is a Lignan isolated from bark, seed cones and leaves of trees of Magnolia species. Honokiol was traditionally used for anxiety and stroke treatment, as well as the alleviation of flu symptoms.
-considered to have antioxidant properties
-low oral bioavailability and difficulty in intravenous administration
-the development of various formulations of honokiol, including microemulsion, liposomes, nanoparticles and micelle copolymers have successfully solved the problem of low water solubility.

Pathways:
-Inhibit NF-κB activation
-Downregulate STAT3 signalin
-Inhibiting the PI3K/Akt pathway,
-Inhibition of mTOR
-Influences various MAPK cascades—including ERK, JNK, and p38
-Inhibition of EGFR
-Inhibiting Notch pathway (CSCs)
-GPx4 inhibit
-Can induce ER stress in cancer cells, which contributes to the activation of unfolded protein response (UPR) pathways
-Disrupt the mitochondrial membrane potential in cancer cells.
-Reported to increase ROS production in cancer cells
-Can exhibit antioxidant properties in normal cells. - has some inhibitor activity but Not classified as HDAC inhibitor as weaker and may work more indirectly.
- is well-known in the research community for its role in activating SIRT3

-Note half-life 40–60 minutes
BioAv
Pathways:
- induce ROS production in cancer cells, and typically lowers ROS in normal cells
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓ Prx
- Raises 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↓, MMPs↓, MMP2↓, MMP9↓, VEGF↓, ROCK1↓, RhoA↓, NF-κB↓, CXCR4↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, EZH2↓, P53↑, HSP↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, EGFR↓,
- inhibits Cancer Stem Cells : CSC↓, CD133↓, β-catenin↓, sox2↓, nestin↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, TrxR**, - Shown to modulate the nuclear translocation of SREBP-2 (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Honokiol — a small, lipophilic biphenolic neolignan isolated principally from the bark, seed cones, and leaves of Magnolia species, especially Magnolia officinalis. It is a natural-product small molecule rather than a standardized Magnolia extract; the standard abbreviation is HNK. Honokiol crosses biological membranes readily and has documented CNS penetration, but its pharmaceutical development is constrained by extremely poor aqueous solubility, rapid metabolism, and low/variable oral systemic exposure. Cancer research is dominated by cell and animal studies, although an oral Phase I window-of-opportunity study in patients with resectable early-stage non-small-cell lung cancer is now enrolling.

Primary mechanisms (ranked):

Mitochondrial targeting and respiratory Complex I inhibition, producing mitochondrial dysfunction, loss of membrane potential, energetic stress, and intrinsic apoptosis in susceptible cancer cells.
Suppression of oncogenic survival signaling, particularly STAT3 and PI3K/AKT/mTOR, with additional inhibition of EGFR and context-dependent MAPK signaling.
Induction of mitochondrial ROS and oxidative stress in cancer cells as a major stress-amplifying mechanism; in nonmalignant tissues honokiol can instead activate antioxidant and mitochondrial-protective programs including SIRT3 and NRF2.
Suppression of NF-κB-dependent inflammatory and prosurvival transcription, contributing to apoptosis, reduced inflammatory signaling, and treatment sensitization.
Suppression of EMT, migration, invasion, cancer-stem-cell phenotypes, and angiogenic signaling through STAT3, Wnt/β-catenin, EGFR, HIF-1α, VEGF, Snail/Slug, MMPs, and related networks.
Metabolic inhibition, including suppression of HIF-1α-driven glycolysis, GLUT1, HK2, LDHA and PDK signaling, with reduced glycolytic flux and ATP availability in several tumor models.
Induction of ER stress, autophagy, cell-cycle arrest and, in selected tumor contexts, ferroptosis; these effects appear downstream or context-dependent rather than universal initiating mechanisms.
Chemosensitization, radiosensitization and immune-modulatory effects have been demonstrated preclinically, including enhancement of selected targeted therapies and PD-1/PD-L1-directed approaches.

Bioavailability / PK relevance: Native honokiol is highly lipophilic and poorly water-soluble, limiting conventional oral and intravenous delivery. It undergoes extensive metabolic clearance, including conjugation, and systemic exposure after ordinary oral formulations may be substantially lower than concentrations commonly used experimentally. Liposomes, nanoemulsions, micelles, nanoparticles and other delivery systems can substantially improve solubility and exposure. A validated pharmacokinetic study of injectable liposomal honokiol has been reported, but clinically established human anticancer PK targets have not yet been defined.

In-vitro vs systemic exposure relevance: Many anticancer studies use approximately 10–60 µM honokiol, with some models requiring still higher concentrations. These concentrations should not automatically be considered achievable following conventional oral supplementation because oral bioavailability is limited and human tumor exposure has not been established. The current Phase I lung-cancer study is therefore important for defining human tolerability, systemic exposure and pharmacodynamic effects rather than demonstrating established therapeutic efficacy.

Clinical evidence status: Predominantly preclinical. Extensive in-vitro and animal anticancer evidence exists across multiple tumor types. Human anticancer efficacy has not been established. A Phase I oral honokiol study in approximately 15 patients with early-stage resectable NSCLC is currently listed by Houston Methodist as enrolling; treatment is given before surgery primarily to determine safety and maximum tolerated dose. Honokiol is not an FDA-approved anticancer drug.

Safety / translation: Preclinical toxicology has generally suggested a comparatively broad therapeutic window, but concentrated honokiol should not be assumed equivalent to historical consumption of Magnolia bark preparations. Potential pharmacokinetic interactions, formulation-dependent exposure, and insufficient controlled human safety data remain major translational limitations. FDA records identify Magnolia cortex extract containing honokiol as having been submitted through the New Dietary Ingredient notification process, but this does not constitute approval of honokiol for cancer treatment.

Honokiol Cancer-Relevant Mechanisms

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	Mitochondrial Complex I and intrinsic apoptosis	↓ Complex I; ↓ ΔΨm; ↓ respiration; ↑ cytochrome-c; ↑ caspases	↔ or mitochondrial protection (context-dependent)	P/R	Mitochondria-directed cytotoxicity	A particularly strong mechanistic feature of honokiol; mitochondrial accumulation and respiratory inhibition can precede downstream apoptotic signaling.
2	STAT3 survival and stemness signaling	↓ STAT3; ↓ p-STAT3; ↓ mitochondrial STAT3	↔ (context-dependent)	R/G	Loss of survival, proliferation and stemness signaling	Relevant across several cancer models and linked to reduced CSC phenotype, EMT and resistance.
3	PI3K AKT mTOR signaling	↓ PI3K; ↓ AKT; ↓ mTOR	↔ or adaptive modulation	R/G	Growth and anabolic suppression	Frequently observed and contributes to apoptosis, metabolic stress and treatment sensitization.
4	Mitochondrial ROS increase	↑ ROS; ↑ mt-ROS (secondary)	↓ ROS or ↔ (context-dependent)	P/R	Oxidative stress amplification	Cancer-cell ROS elevation often accompanies mitochondrial respiratory disruption. Honokiol can instead act antioxidatively in nonmalignant tissues.
5	NF-κB inflammatory and survival signaling	↓ NF-κB; ↓ COX-2; ↓ inflammatory survival signaling	↓ pathological inflammatory signaling	R/G	Reduced inflammatory and prosurvival transcription	Provides both anticancer and tissue-protective effects depending on cellular context.
6	EMT invasion and metastasis	↓ EMT; ↓ Snail; ↓ Slug; ↓ MMP2; ↓ MMP9; ↑ E-cadherin	↔	G	Reduced migration, invasion and metastasis	Supported across breast, lung, renal, pancreatic and other tumor models.
7	Cancer stem cell signaling	↓ CSCs; ↓ CD133; ↓ SOX2; ↓ OCT4; ↓ Nestin; ↓ Wnt/β-catenin	↔	G	Reduced tumor-initiating and resistant cell phenotype	Closely overlaps STAT3, EGFR, Notch and Wnt pathway inhibition.
8	HIF-1α glycolytic metabolism	↓ HIF-1α; ↓ GLUT1; ↓ HK2; ↓ LDHA; ↓ PDK1; ↓ ECAR; ↓ glycolysis	↔ (context-dependent)	G	Reduced glycolytic flux and ATP production	Especially relevant in glycolysis-dependent and hypoxic tumors.
9	EGFR and receptor tyrosine kinase signaling	↓ EGFR; ↓ downstream AKT and ERK	↔	R/G	Growth-factor signal suppression	Honokiol can also impair EGFR stability through HDAC6/HSP90-associated mechanisms.
10	Angiogenesis and hypoxia response	↓ VEGF; ↓ HIF-1α; ↓ angiogenesis	↔	G	Reduced tumor vascular support	Largely downstream of HIF-1α, NF-κB and growth-factor suppression.
11	ER stress and calcium signaling	↑ ER stress; ↑ GRP78; ↑ CHOP; ↑ Ca²⁺ (model-dependent)	↔ or protective stress response	R/G	Proteotoxic stress and apoptosis	Prominent in selected osteosarcoma and other experimental models rather than universal across cancers.
12	Cell cycle regulation	↑ G0/G1 or G2/M arrest; ↓ cyclin D1; ↓ CDK2; ↓ CDK4; ↓ CDK6	↔	G	Cytostatic growth suppression	Checkpoint phenotype depends on tumor type and upstream signaling context.
13	Ferroptosis and lipid peroxidation	↑ ferroptosis; ↑ lipid peroxidation; GPX4 modulation (model-dependent)	↔	G	Alternative regulated cell death	GPX4 direction is not uniform across studies; HMOX1-associated and GPX4-associated ferroptosis have both been reported.
14	NRF2 antioxidant response	↔ or ↑ (model-dependent)	↑ NRF2; ↑ antioxidant defenses	R/G	Secondary tissue-protective redox response	NRF2 activation is more compelling as a normal-cell or neuroprotective mechanism than as a core anticancer mechanism.
15	SIRT3 mitochondrial protection	↑ SIRT3 (context-dependent)	↑ SIRT3; ↑ mitochondrial resilience; ↓ oxidative injury	R/G	Context-dependent mitochondrial regulation	Important for cardioprotective and neuroprotective effects; its cancer role can vary with tumor context because SIRT3 itself has context-dependent tumor biology.
16	Chemosensitization and targeted-therapy sensitization	↑ treatment sensitivity (drug-dependent)	↔ or tissue protection	G	Combination-treatment enhancement	Preclinical evidence includes chemotherapy, cetuximab, mTOR inhibitors and immune-checkpoint strategies.
17	Radiosensitization	↑ radiosensitivity (model-dependent)	↔ or radioprotection (context-dependent)	G	Greater radiation response	This apparent duality emphasizes cell type, dose, redox state and treatment timing.
18	Clinical Translation Constraint	↓ achievable exposure with conventional formulations	Systemic safety incompletely characterized in humans	G	Bioavailability and evidence limitation	Poor aqueous solubility, extensive metabolism, uncertain human tumor exposure and lack of efficacy trials remain central constraints; Phase I investigation is underway.

P: 0–30 min R: 30 min–3 hr G: >3 hr

Honokiol and Alzheimer’s disease: Honokiol has meaningful but entirely preclinical relevance to Alzheimer’s disease and related neurodegeneration. Its lipophilicity permits CNS penetration, and experimental studies indicate reductions in oxidative stress, neuroinflammation, excitotoxicity and Aβ-associated toxicity together with preservation of mitochondrial function. SIRT3, NRF2, PPAR/PGC-1α signaling and restoration of microglial metabolic competence are among the more plausible mechanistic axes. No convincing clinical evidence currently establishes honokiol as an AD treatment.

Evidence level: Preclinical only. Cell and animal studies support neuroprotective and cognition-related effects, but human AD efficacy, dose-response relationships and long-term neurological safety have not been demonstrated.

Honokiol Alzheimer’s-Relevant Mechanisms

Rank	Pathway / Axis	Modulation	Primary Effect	Notes / Interpretation
1	Mitochondrial function and SIRT3	↑ SIRT3; ↑ mitochondrial function; ↑ ΔΨm	Mitochondrial resilience	One of the strongest mechanistic links between honokiol and neuronal protection.
2	Oxidative stress and NRF2	↓ ROS; ↑ NRF2; ↑ antioxidant defenses	Reduced oxidative injury	Direction differs from the pro-oxidant stress frequently induced by honokiol in cancer cells.
3	Microglial metabolism and phagocytosis	↑ PPARα; ↑ PGC-1α; ↑ OXPHOS; ↑ phagocytosis	Improved microglial metabolic function	Experimental evidence suggests reversal of dysfunctional metabolic programming can restore microglial clearance capacity.
4	Amyloid beta toxicity	↓ Aβ-associated toxicity	Neuroprotection	Supported primarily by experimental models; evidence for modifying human amyloid pathology is absent.
5	Neuroinflammation	↓ NF-κB; ↓ TNF-α; ↓ IL-1β	Reduced inflammatory injury	Likely overlaps the general anti-inflammatory pharmacology of honokiol.
6	Excitotoxic calcium signaling	↓ pathological Ca²⁺ signaling	Reduced excitotoxic neuronal injury	Reported neuroprotective actions include modulation of glutamatergic signaling and intracellular calcium overload.
7	Clinical Translation Constraint	No demonstrated human AD efficacy	Preclinical evidence only	BBB penetration is pharmacologically favorable but does not establish an effective or safe human CNS dose.

RadioS, RadioSensitizer: Click to Expand ⟱

Source:

Type:

A radiosensitizer is an agent that makes cancer cells more sensitive to the damaging effects of radiation therapy. By using a radiosensitizer, clinicians aim to enhance the effectiveness of radiation treatment by either increasing the damage incurred by tumor cells or by interfering with the cancer cells’ repair mechanisms. This can potentially allow for lower doses of radiation, reduced side effects, or improved treatment outcomes.
Pathways that help Radiosensitivity: downregulating HIF-1α, increase SIRT1, Txr

List of Natural Products with radiosensitizing properties:
-Curcumin:modulate NF-κB, STAT3 and has been shown in preclinical studies to enhance the effects of radiation by inhibiting cell survival pathways.
-Resveratrol:
-EGCG:
-Quercetin:
-Genistein:
-Parthenolide:

How radiosensitizers inhibit the thioredoxin (Trx) system in cellular contexts. Notable radiosensitizers, including:
-gold nanoparticles (GNPs),
-gold triethylphosphine cyanide ([Au(SCN) (PEt3)]),
-auranofin, ceria nanoparticles (CONPs),
-curcumin and its derivatives,
-piperlongamide,
-indolequinone derivatives,
-micheliolide,
-motexafin gadolinium, and
-ethane selenide selenidazole derivatives (SeDs)

Scientific Papers found: Click to Expand⟱

2896-

HNK,

Honokiol inhibits hypoxia-inducible factor-1 pathway

in-vivo,

Colon,

CT26

subcutaneous murine colon carcinoma, CT26

Hif1a↓, Our data suggest that honokiol can exert its anticancer activity as a HIF-1α inhibitor by reducing HIF-1α protein level and suppressing the hypoxia-related signaling pathway.
RadioS↑, The animal experiment indicates that honokiol improves the therapeutic efficacy of radiation

4522-

HNK,

MAG,

Honokiol Is More Potent than Magnolol in Reducing Head and Neck Cancer Cell Growth

in-vitro,

HNSCC,

FaDu

AntiCan↑, Natural compounds, like Magnolia-derived lignans—honokiol (HON) and magnolol (MAG)—can reduce cancer cell growth but retain a good safety profile and thus may show benefit as adjuvant therapeutics.
tumCV↓, We observed that HON and MAG were more potent in reducing cell viability in cisplatin persister FaDu cells, although this effect was not directly followed by increased rates of apoptosis.
eff↑, we observed that HON exerted stronger cytotoxic effects than MAG in HNSCC cells, and the difference in their anti-cancer activity was especially pronounced in cells cultured in 3D.
survivin↓, HON improved the effects of radiotherapy by targeting survivin, as shown in the in vitro and xenograft models of HNSCC
RadioS↑,

2885-

HNK,

Honokiol: a novel natural agent for cancer prevention and therapy

NF-kB↓, Honokiol targets multiple signaling pathways including nuclear factor kappa B (NF-κB), signal transducers and activator of transcription 3 (STAT3), epidermal growth factor receptor (EGFR) and mammalian target of rapamycin (m-TOR)
STAT3↓,
EGFR↓,
mTOR↓,
BioAv↝, honokiol has revealed a desirable spectrum of bioavailability after intravenous administration in animal models, thus making it a suitable agent for clinical trials
Inflam↓, inflammation, proliferation, angiogenesis, invasion and metastasis.
TumCP↓,
angioG↓,
TumCI↓,
TumMeta↓,
cSrc↓, STAT3 inhibition by honokiol has also been correlated with the repression of upstream protein tyrosine kinases c-Src, JAK1 and JAK2
JAK1↓,
JAK2↓,
ERK↓, by inhibiting ERK and Akt pathways (31) or by upregulation of PTEN
Akt↓,
PTEN↑,
ChemoSen↑, Chemopreventive/ chemotherapeutic effects of honokiol in various malignancies: preclinical studies
chemoP↑,
COX2/PTGS2↓, honokiol was found to inhibit UVB-induced expression of cyclooxygenase-2, prostaglandin E2, proliferating cell nuclear antigen and pro-inflammatory cytokines, such as TNF-α, interleukin (IL)-1β and IL-6 in the skin
PGE2↓,
TNF-α↓,
IL1β↓,
IL6↓,
Casp3↑, release of caspases-3, -8 and -9as well as poly (ADP-ribose) polymerase (PARP) cleavage and p53 activation upon honokiol treatment that led to DNA fragmentation
Casp8↑,
Casp9↑,
cl‑PARP↑,
DNAdam↑,
Cyt‑c↑, translocation of cytochrome c to cytosol in human melanoma cell lines
RadioS↑, liposomal honokiol for 24 h showed a higher radiation enhancement ratio (~ two-fold) as compared to the radiation alone,
RAS↓, Honokiol also caused suppression of Ras activation
BBB↑, honokiol could effectively cross BBB and BCSFB and inhibit brain tumor growth
BioAv↓, Due to the concerns about poor aqueous solubility, liposomal formulations of honokiol have been developed and tested for their pharmacokinetics
Half-Life↝, In another comparative study, plasma honokiol concentrations was maintained above 30 and 10 μg/mL for 24 and 48 hours, respectively, in liposomal honokiol-treated mice, whereas it fell quickly (less than 5 μg/mL) by 12 hours in free honokiol-treated
Half-Life↝, free honokiol has poor GIT absorption, bio-transformed in liver to mono-glucuronide honokiol and sulphated mono-hydroxyhonokiol, ~ 50% is secreted in bile, ~ 60-65% plasma protein bound with elimination half life of (t1/2) of 49.05 – 56.24 minutes.
toxicity↓, These studies suggest that honokiol either alone or as a part of magnolia bark extract does not induce toxicity in animal models and thus could be clinically safe

2883-

HNK,

Honokiol targets mitochondria to halt cancer progression and metastasis

Review,

Var,

ChemoSen↑, Combination of HNK with many traditional chemotherapeutic drugs as well as radiation sensitizes cancer cells to apoptotic death
BBB↓, HNK is also capable of crossing the BBB
Ca+2↑, HNK promotes human glioblastoma cancer cell apoptosis via regulation of Ca(2+) channels
Cyt‑c↑, release of mitochondrial cytochrome c and activation of caspase-3
Casp3↑,
chemoPv↑, potent chemopreventive agent against lung SCC development in a carcinogen-induced lung SCC murine model
OCR↓, HNK treatment results in a decreased oxygen consumption rate (OCR) in whole intact cells, rapidly, and persistently inhibiting mitochondrial respiration, which leads to the induction of apoptosis
mitResp↓,
Apoptosis↑,
RadioS↑, Honokiol as a chemo- and radiosensitizer
NF-kB↓, HNK as an anticancer drug is its potential to inhibit multiple important survival pathways, such as NF-B and Akt
Akt↓,
TNF-α↓, by inhibiting TNF-induced nerve growth factor IB expression in breast cancer cells
PGE2↓, reduced prostaglandin E2 (PGE2) and vascular endothelial growth factor (VEGF) secretion levels
VEGF↓,
NO↝, HNK inhibits cancer cell migration by targeting nitric oxide and cyclooxygenase-2 or Ras GTPase-activating-like protein (IQGAP1) [
COX2/PTGS2↓,
RAS↓,
EMT↓, HNK can reverse the epithelial-mesenchymal-transition (EMT) process, which is a key step during embryogenesis, cancer invasion, and metastasis,
Snail↓, HNK reduced the expression levels of Snail, N-cadherin and -catenin, which are mesenchymal markers, but increased E-cadherin,
N-cadherin↓,
β-catenin/ZEB1↓,
E-cadherin↑,
ER Stress↑, induction of ER stress
p‑STAT3↓, HNK inhibited STAT3 phosphorylation
EGFR↓, inhibiting EGFR phosphorylation and its downstream signaling pathways such as the mTOR signaling pathway
mTOR↓,
mt-ROS↑, We demonstrated that HNK treatment suppresses mitochondrial respiration and increases generation of ROS in the mitochondria, leading to the induction of apoptosis in lung cancer cells
PI3K↓, inhibition of PI3K/Akt/ mTOR, EMT, and Wnt signaling pathways.
Wnt↓,

Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: RadioS, RadioSensitizer

4 Honokiol
1 Magnolol

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#:94  Target#:1107  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Honokiol / RadioS Cancer Research Results

Honokiol Cancer-Relevant Mechanisms

Honokiol Alzheimer’s-Relevant Mechanisms

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

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