| 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 |
| Source: |
| Type: |
| The selectivity of cancer products (such as chemotherapeutic agents, targeted therapies, immunotherapies, and novel cancer drugs) refers to their ability to affect cancer cells preferentially over normal, healthy cells. High selectivity is important because it can lead to better patient outcomes by reducing side effects and minimizing damage to normal tissues. Achieving high selectivity in cancer treatment is crucial for improving patient outcomes. It relies on pinpointing molecular differences between cancerous and normal cells, designing drugs or delivery systems that exploit these differences, and overcoming intrinsic challenges like tumor heterogeneity and resistance Factors that affect selectivity: 1. Ability of Cancer cells to preferentially absorb a product/drug -EPR-enhanced permeability and retention of cancer cells -nanoparticle formations/carriers may target cancer cells over normal cells -Liposomal formations. Also negatively/positively charged affects absorbtion 2. Product/drug effect may be different for normal vs cancer cells - hypoxia - transition metal content levels (iron/copper) change probability of fenton reaction. - pH levels - antiOxidant levels and defense levels 3. Bio-availability |
| 2879- | HNK, | Honokiol Inhibits Lung Tumorigenesis through Inhibition of Mitochondrial Function |
| - | in-vitro, | Lung, | H226 | - | in-vivo, | NA, | NA |
| 2875- | HNK, | Inhibition of class I histone deacetylases in non-small cell lung cancer by honokiol leads to suppression of cancer cell growth and induction of cell death in vitro and in vivo |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Lung, | H1299 | - | in-vitro, | Lung, | H460 | - | in-vitro, | SCC, | H226 |
| 2891- | HNK, | Honokiol, an Active Compound of Magnolia Plant, Inhibits Growth, and Progression of Cancers of Different Organs |
| - | Review, | Var, | NA |
| 2892- | HNK, | Honokiol Induces Apoptosis, G1 Arrest, and Autophagy in KRAS Mutant Lung Cancer Cells |
| - | in-vitro, | Lung, | A549 | - | in-vitro, | Lung, | H460 | - | in-vitro, | Lung, | H385 | - | in-vitro, | Nor, | BEAS-2B |
| 2895- | HNK, | Mitochondria-Targeted Honokiol Confers a Striking Inhibitory Effect on Lung Cancer via Inhibiting Complex I Activity |
| - | in-vitro, | Lung, | PC9 |
| 2073- | HNK, | Honokiol induces apoptosis and autophagy via the ROS/ERK1/2 signaling pathway in human osteosarcoma cells in vitro and in vivo |
| - | in-vitro, | OS, | U2OS | - | in-vivo, | NA, | NA |
| 2864- | HNK, | Honokiol: A Review of Its Anticancer Potential and Mechanisms |
| - | Review, | Var, | NA |
| 2865- | HNK, | Liposomal Honokiol induces ROS-mediated apoptosis via regulation of ERK/p38-MAPK signaling and autophagic inhibition in human medulloblastoma |
| - | in-vitro, | MB, | DAOY | - | vitro+vivo, | NA, | NA |
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