Isobavachalcone / ROS Cancer Research Results

IBC, Isobavachalcone: Click to Expand ⟱

Features:

Isobavachalcone - Prenylated Chalcone

Type: Natural prenylated chalcone / flavonoid-related phytochemical
-Chalcone → chemical class / parent scaffold, not a molecular target. -Example Chalones: Isobavachalcone, xanthohumol, licochalcone A, isoliquiritigenin

Sources: Found in several medicinal plants, particularly Psoralea corylifolia (Cullen corylifolium), as well as other plant species containing prenylated chalcones.

Function: Isobavachalcone is a bioactive prenylated chalcone with anticancer, anti-inflammatory, antioxidant, antimicrobial, and neuroprotective activities. Reported molecular effects include modulation of AKT, ERK/MAPK, ROS, apoptosis, inflammatory signaling, and cellular stress pathways.

Cancer: Experimental studies demonstrate inhibition of cancer-cell proliferation, migration, and invasion and induction of apoptosis and other forms of regulated cell death. IBC can suppress AKT and ERK signaling, increase tumor-cell oxidative stress, and modulate antitumor immune responses. Anticancer activity has been demonstrated in pancreatic, breast, oral, colorectal, thyroid, and other experimental cancer models.

Alzheimer's Disease: Preclinical studies indicate neuroprotective activity, including reduction of Aβ accumulation and plaque pathology, suppression of neuroinflammation, and improvement of memory and cognitive deficits in Alzheimer's disease models.

Isobavachalcone — Isobavachalcone (IBC; CAS 20784-50-3) is a naturally occurring prenylated chalcone and flavonoid-related phytochemical found particularly in Psoralea corylifolia L. (syn. Cullen corylifolium; Psoraleae Fructus/Bu Gu Zhi). It is an experimental small-molecule natural product with anticancer, anti-inflammatory, antimicrobial, and neuroprotective activities. Current anticancer evidence is preclinical and increasingly supports direct or proximal effects on SIRT2, DHODH, thioredoxin reductase 1, AKT signaling, mitochondrial function, and redox homeostasis. IBC has not been established as an approved anticancer or Alzheimer therapy.

Primary mechanisms (ranked):

Mitochondrial and redox disruption with ↑ ROS, mitochondrial membrane depolarization, impaired respiration/ATP production, mitochondrial Ca²⁺ overload, and activation of mitochondrial permeability-transition-associated cell death.
↓ AKT signaling, including direct inhibition of AKT1 activity in early studies and suppression of AKT phosphorylation, reducing survival signaling and promoting mitochondrial apoptosis.
Direct ↓ SIRT2 activity, disrupting SIRT2/α-tubulin signaling and downstream STAT3/c-Myc and Snail/MMP pathways in triple-negative breast cancer.
↓ DHODH with mitochondrial dysfunction, mtDNA release, ↑ ROS, and activation of cGAS-STING-associated antitumor immunity in gastric cancer models.
↓ thioredoxin reductase 1, weakening cellular thioredoxin antioxidant capacity and promoting ROS-dependent ER stress and apoptosis in prostate cancer.
Induction of multiple regulated cell-death programs including mitochondrial apoptosis, non-canonical mitochondrial permeability-transition-driven necrosis, pyroptosis, necroptosis, and autophagy, depending on tumor model.
Suppression of invasion and metastatic signaling through pathways including ↓ β-catenin, ↓ MMP-2/MMP-9, ↓ Snail, and other context-dependent AKT/GSK-3β/β-catenin and SIRT2-associated mechanisms.
Antitumor immune modulation, including ↑ CD8+ T-cell infiltration, ↓ M2 macrophage polarization, and STING-associated innate immune activation in animal tumor models.
ABCB1 modulation and membrane perturbation, potentially increasing drug accumulation in some multidrug-resistant cancer cells.
Secondary NRF2/HO-1 activation has been reported primarily in anti-inflammatory/non-cancer contexts and should not be interpreted as the principal anticancer mechanism.

Bioavailability / PK relevance: Human pharmacokinetics have not been established. Rat oral pharmacokinetic studies demonstrate measurable systemic exposure after high oral dosing, but IBC undergoes extensive glucuronidation involving UGT1A1, UGT1A3 and additional UGT isoforms, with BCRP/MRP-mediated glucuronide efflux. These metabolic characteristics may limit free systemic exposure. IBC also inhibits multiple CYP and UGT enzymes in vitro at low-micromolar concentrations, creating a potential drug-interaction concern if therapeutically relevant human exposure can be achieved.

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately low- to several-tens-of-micromolar IBC concentrations; for example, MCF-7 growth inhibition has been reported at IC50 values around 28–38 µM, whereas direct SIRT2 inhibition occurs at substantially lower concentrations with an enzymatic IC50 of approximately 0.84 µM. Human plasma concentrations after oral dosing are unknown, so it cannot currently be assumed that the concentrations required for many cell-culture anticancer effects are clinically achievable. High-concentration mitochondrial ROS effects are particularly relevant to the hepatotoxicity signal and may narrow any therapeutic window.

Clinical evidence status: Preclinical. Anticancer activity has been demonstrated in numerous cancer cell systems and several mouse xenograft/allograft models, including breast, gastric, pancreatic, colorectal, prostate, AML, thyroid, and other cancers. No established human anticancer efficacy, therapeutic dose, validated exposure-response relationship, or regulatory approval has been demonstrated.

Safety: Hepatotoxicity is a significant translational constraint. IBC itself has produced mitochondrial dysfunction, ROS accumulation, loss of mitochondrial membrane potential, ATP depletion, apoptosis, and ferroptosis-associated injury in hepatic experimental systems. Psoralea corylifolia preparations are independently associated with clinically reported liver injury, although toxicity of the whole herb cannot be attributed exclusively to IBC. Potential CYP/UGT inhibition further raises concern for pharmacokinetic drug interactions.

Isobavachalcone Cancer-Relevant Mechanisms

Rank	Pathway / Axis	Cancer Cells	Normal Cells	Primary Effect	Notes / Interpretation
1	Mitochondrial ROS and bioenergetic disruption	↑ ROS; ↓ mitochondrial membrane potential; ↓ respiration; ↓ ATP	Similar mitochondrial toxicity can occur in hepatocytes	Metabolic collapse and cell death	Central recurring mechanism across multiple cancer models, but lack of strict tumor selectivity is an important safety limitation.
2	AKT survival signaling	↓ AKT activity; ↓ p-AKT	↓ p-AKT reported during hepatic toxicity	↓ survival signaling; ↑ apoptosis	IBC has been reported to inhibit AKT1 kinase and repeatedly suppress cellular AKT phosphorylation.
3	Mitochondrial permeability transition and Ca²⁺	↑ mitochondrial Ca²⁺; ↑ pore opening; ↓ membrane potential	Not well characterized	↑ regulated necrosis	ROS-dependent non-canonical mitochondrial permeability-transition-driven necrosis demonstrated in breast and lung cancer models.
4	SIRT2 signaling	↓ SIRT2; ↑ α-tubulin acetylation; ↓ STAT3/c-Myc; ↓ Snail/MMP signaling	Limited comparative data	↓ proliferation and migration; ↑ apoptosis	Direct SIRT2 inhibition reported with an enzymatic IC50 of approximately 0.84 µM in TNBC studies.
5	DHODH mitochondrial pyrimidine metabolism	↓ DHODH; ↑ ROS; ↑ mitochondrial damage; ↑ mtDNA release	Limited comparative data	Metabolic stress and antitumor immune activation	Recent gastric-cancer evidence identifies DHODH as a functional target linking mitochondrial injury with STING signaling.
6	cGAS-STING innate immune signaling	↑ STING-associated signaling	Context-dependent	↑ antitumor immune response	Associated with mitochondrial damage and mtDNA release in gastric-cancer models.
7	Thioredoxin reductase 1 redox defense	↓ TrxR1; ↑ ROS; ↑ ER stress	Potential oxidative toxicity	↑ apoptosis	TrxR1 has been proposed as a direct redox-sensitive IBC target in prostate cancer cells.
8	Mitochondrial apoptosis	↑ Bax; ↓ Bcl-2/Bcl-xL/Mcl-1; ↑ cytochrome c; ↑ caspase-9/3; ↑ PARP cleavage	Can also occur in hepatic cells	↑ apoptosis	Highly reproducible downstream phenotype in several tumor types.
9	Pyroptosis	↑ caspase-dependent GSDME cleavage	Insufficient comparative data	↑ inflammatory cell death	Demonstrated particularly in anaplastic thyroid cancer models.
10	Necroptosis and autophagy	↑ RIP3/MLKL signaling; ↑ LC3-II/I (model-dependent)	Context-dependent	Multiple regulated cell-death responses	Observed in selected breast-cancer models; not a universal IBC response.
11	AKT GSK-3β β-catenin signaling	↓ pathway activity	Not well characterized	↓ proliferation and survival	Reported prominently in colorectal cancer cells.
12	Migration and extracellular matrix remodeling	↓ MMP-2; ↓ MMP-9; ↓ Snail; ↓ migration/invasion	Limited data	↓ invasive phenotype	Supported in oral, breast, colorectal, and related cancer models.
13	Tumor immune microenvironment	↑ CD8+ T cells; ↓ M2 macrophages	Immune modulation is context-dependent	↑ antitumor immunity	Demonstrated in orthotopic pancreatic tumor models.
14	ABCB1 multidrug resistance	↓ ABCB1 transport function (context-dependent)	May alter xenobiotic transport	Potential chemosensitization	IBC behaves as a membrane-active ABCB1 substrate and/or competitive inhibitor; clinical chemosensitization has not been established.
15	NRF2 HO-1 antioxidant signaling	Context-dependent	↑ NRF2/HO-1 reported mainly in inflammatory models	Anti-inflammatory and cytoprotective effects	Secondary mechanism and potentially opposite to the desired pro-oxidant anticancer state.
16	Clinical Translation Constraint	Effective concentrations frequently in low-to-tens-of-µM range	Hepatic mitochondrial and ferroptotic toxicity documented experimentally	Limits therapeutic translation	Human PK, therapeutic exposure, tumor selectivity, maximum tolerated dose, and clinical efficacy remain undefined; extensive glucuronidation and CYP/UGT interactions are additional constraints.

Alzheimer's disease relevance: Isobavachalcone has meaningful but exclusively preclinical evidence in Alzheimer's disease. In transgenic AD mouse models, IBC has improved memory-related outcomes and reduced Aβ pathology, tau hyperphosphorylation, and neuroinflammation. More recent work links these effects to ↑ autophagic Aβ clearance and ↓ NLRP3 inflammasome activation in astrocytes. Earlier studies also identified inhibitory activity against several AD-associated targets, including Aβ42-related processes, BACE1, GSK-3β, and acetylcholinesterase. No human efficacy, dose, pharmacokinetic target, or clinical safety data support its use for AD.

Isobavachalcone Alzheimer-Relevant Mechanisms

Rank	Pathway / Axis	Modulation	Primary Effect	Notes / Interpretation
1	Amyloid beta clearance	↓ Aβ accumulation and plaque burden	Reduced amyloid pathology	Supported in transgenic mouse models.
2	Autophagy	↑ autophagic clearance	↑ Aβ removal	Mechanistically supported in primary astrocytes and 5xFAD mice.
3	NLRP3 inflammasome	↓ NLRP3 activation	↓ neuroinflammation	Astrocyte-associated anti-inflammatory mechanism demonstrated in recent preclinical work.
4	Tau pathology	↓ tau hyperphosphorylation and filament formation	Reduced tau pathology	Reported in 3×Tg-AD mice.
5	GSK-3β	↓ activity	Potential reduction of tau phosphorylation	Supported mainly by earlier multi-target biochemical studies.
6	BACE1 and amyloidogenic processing	↓ activity	Potential ↓ Aβ generation	Preclinical biochemical evidence; in-vivo contribution is less certain.
7	Acetylcholinesterase	↓ activity	Potential cholinergic support	Biochemical activity; clinical relevance has not been established.
8	Clinical Translation Constraint	Human exposure and CNS penetration not established	Uncertain therapeutic feasibility	Potential hepatotoxicity, metabolism, drug interactions, and lack of human PK/efficacy are major constraints.

ROS, Reactive Oxygen Species: Click to Expand ⟱

Source: HalifaxProj (inhibit)

Type:

Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy

ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination


Item  ROS↑  NRF2  Condition  Mechanism Class  Remarks  

ROS">Piperlongumine
+++  ↓  [D][T]  ROS-dominant
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



ROS">Copper (ionic / nano)
+++ ↓ [Fe][F] ROS-dominant
Fenton-type redox chemistry



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



ROS">Alpha-lipoic acid (ALA)
± ↑ [D][M] NRF2-dominant
Antioxidant at low dose



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



ROS">Quercetin
± ↑/↓ [D][Fe] NRF2-dominant
GSH-dependent cycling



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

Scientific Papers found: Click to Expand⟱

7775-

IBC,

Isobavachalcone Induces Multiple Cell Death in Human Triple-Negative Breast Cancer MDA-MB-231 Cells

vitro+vivo,

BC,

MDA-MB-231

IBC induced mitochondrial dysfunction, thereby decreasing cellular ATP levels and increasing reactive oxygen species accumulation to induce PCD.

TumCP↓, Apoptosis↑, Necroptosis↑, TumAuto↑, Akt↓, BAX↑, cl‑Casp3↑, RIP3↑, p‑RIP3↑, MLKL↑, LC3‑Ⅱ/LC3‑Ⅰ↑, mtDam↑, ATP↓, ROS↑, TumCG↓,

7805-

IBC,

The enhanced hepatotoxicity of isobavachalcone in depigmented zebrafish due to calcium signaling dysregulation and lipid metabolism disorder

in-vivo,

Nor,

*hepatoP↓, *ROS↑, *Ca+2↝,

7804-

IBC,

Isobavachalcone: A comprehensive review of its plant sources, pharmacokinetics, toxicity, pharmacological activities and related molecular mechanisms

Review,

Nor,

*BioAv↓, *BBB↑, *hepatoP↓, ROS↑, *NA↓, ERK↓, Wnt↓, Apoptosis↑, *NF-kB↓, *NRF2↑, *HO-1↑, *Inflam↓,

7803-

IBC,

Isobavachalcone induces hepatotoxicity in zebrafish embryos and HepG2 cells via the System Xc--GSH-GPX4 signaling pathway in ferroptosis response

in-vivo,

Nor,

Zebrafish

in-vitro,

NA,

HepG2

*hepatoP↓, *ALAT↑, *AST↑, *ROS↑, *MDA↑, *Catalase↓, *GSH↓, *GPx↓, *i-Iron↑,

7802-

IBC,

Isobavachalcone disrupts mitochondrial respiration and induces cytotoxicity through ROS accumulation and Akt suppression

in-vitro,

NA,

HepG2

TumCD↑, Apoptosis↑, ROS↑, mtDam↑, p‑Akt↓, eff↓,

7776-

IBC,

Isobavachalcone Activates Antitumor Immunity on Orthotopic Pancreatic Cancer Model: A Screening and Validation

vitro+vivo,

PC,

Panc02

TumCP↓, Apoptosis↑, ROS↑, TumW↓, CD8+↑, M2 MC↓, CSCs↓, antiNeop↑, Imm↑, eff↓, Bcl-2↓, BAX↑,

7385-

IBC,

Fighting cancer by triggering non-canonical mitochondrial permeability transition-driven necrosis through reactive oxygen species induction

vitro+vivo,

Lung,

A549

in-vitro,

BC,

4T1

Apoptosis↑, necrosis↑, ROS↑, mtDam↑, Ca+2↑, MPT↑, MMP↓, AntiCan↑, *AntiBio↑, *Inflam↓, *antiOx↓, *neuroP↑, p‑Akt↓, DHODH↓, Diff↑, MAPK↑,

7772-

IBC,

Isobavachalcone inhibits acute myeloid leukemia: Potential role for ROS-dependent mitochondrial apoptosis and differentiation

vitro+vivo,

AML,

NOD/SCID mice

Apoptosis↑, Diff↑, tumCV↓, TumCP↓, MMP↓, BAX↑, Bcl-2↓, Bcl-xL↓, Mcl-1↓, Cyt‑c↑, cl‑Casp3↑, cl‑Casp9↑, cl‑PARP↑, p‑MEK↑, p‑ERK↑, ROS↑, eff↓,

7771-

IBC,

Isobavachalcone induces concurrent apoptosis and pyroptosis in anaplastic thyroid cancer cells by modulating the caspase-mediated cleavage of PARP and GSDME

vitro+vivo,

Thyroid,

CAL-62

This <span class="wphighlight">ROS</span> overload subsequently triggers endoplasmic reticulum (ER) stress and induces mitochondria-mediated apoptosis

TumCG↓, TumCCA↑, Apoptosis↑, Pyro↑, Casp↑, cl‑PARP↑, cl‑GSDME↑, TrxR1↓, ROS↑, ER Stress↑, Dose↝,

7770-

IBC,

Fighting cancer by triggering non-canonical mitochondrial permeability transition-driven necrosis through reactive oxygen species induction

in-vitro,

Lung,

vitro+vivo,

BC,

4T1

necrosis↑, ROS↑, mtDam↑, Ca+2↑, NA↑, MMP↓, TumCG↓,

7767-

IBC,

Isobavachalcone exerts anti-gastric cancer effects by targeting dihydroorotate dehydrogenase to induce ROS release and activating the STING pathway

vitro+vivo,

GC,

TumCG↓, ROS↑, DHODH↓, MMP↓, cGAS–STING↑, Imm↑, mtDam↑,

7711-

IBC,

Isobavachalcone, a natural sirtuin 2 inhibitor, exhibits anti-triple-negative breast cancer efficacy in vitro and in vivo

vitro+vivo,

BC,

SIRT2↓, Dose↝, Snail↓, MMPs↓, STAT3↓, cMyc↓, ROS↑,

Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 1,
Total Targets: 57

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1, NA↓, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1, Catalase↓, 1, GPx↓, 1, GSH↓, 1, HO-1↑, 1, i-Iron↑, 1, MDA↑, 1, NRF2↑, 1, ROS↑, 2,

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↑, 1,

Migration(tgid=13) ⓘ

Ca+2↝, 1,

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 2, NF-kB↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,

Clinical Biomarkers(tgid=22) ⓘ

ALAT↑, 1, AST↑, 1,

Functional Outcomes(tgid=23) ⓘ

hepatoP↓, 3, neuroP↑, 1,
Total Targets: 21

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

12 Isobavachalcone

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#:446  Target#:275  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

Isobavachalcone / ROS Cancer Research Results

Isobavachalcone Cancer-Relevant Mechanisms

Isobavachalcone Alzheimer-Relevant Mechanisms

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Migration(tgid=13) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

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