Betulinic acid / GRP78/BiP Cancer Research Results

BetA, Betulinic acid: Click to Expand ⟱
Features:
Betulinic acid "buh-TOO-li-nik acid" is a natural compound with antiretroviral, anti malarial, anti-inflammatory and anticancer properties. It is found in the bark of several plants, such as white birch, ber tree and rosemary, and has a complex mode of action against tumor cells.
-Betulinic acid is a naturally occurring pentacyclic triterpenoid
-vitro concentrations range from 1–100 µM, in vivo studies in rodents have generally used doses from 10–100 mg/kg
Precursor: Betulin, via oxidation at C-28
Lipophilicity: High (poor aqueous solubility)

Betulinic acid — Betulinic acid is a naturally occurring lupane-type pentacyclic triterpenoid with broad experimental anticancer activity, especially against melanoma, neuroectodermal, glioma, breast, colorectal, and other solid-tumor models. It is a natural-product small molecule, usually abbreviated BA or BetA, and is found in several plants, classically birch bark, with semi-synthesis commonly starting from betulin. A distinguishing feature is preferential induction of tumor-cell death through direct mitochondrial injury with relative sparing of many non-neoplastic cells in preclinical systems. Its main translational limitation is very poor aqueous solubility with correspondingly weak oral/systemic developability unless formulation or derivatization is used.

Primary mechanisms (ranked):

  1. Direct mitochondrial membrane permeabilization with intrinsic apoptosis activation
  2. Mitochondrial ROS increase with collapse of mitochondrial membrane potential and cytochrome c release
  3. ER-stress and unfolded-protein-response activation, including GRP78-linked stress signaling
  4. Suppression of NF-κB and other pro-survival transcriptional programs, including Sp-family signaling in some models
  5. Cell-cycle arrest with reduced cyclin/CDK signaling
  6. Anti-migratory and anti-invasive effects via EMT, FAK, ROCK1, MMP, and cytoskeletal remodeling pathways
  7. Secondary metabolic suppression of aerobic glycolysis and hypoxia-response signaling in susceptible models
  8. Adjunct sensitization to chemo- or radiotherapy in selected preclinical settings

Bioavailability / PK relevance: Betulinic acid is highly lipophilic and poorly water-soluble, which strongly limits oral absorption and systemic exposure. PK behavior is formulation-dependent, and much of the translational literature focuses on nanoparticles, liposomes, micelles, conjugates, or topical delivery rather than conventional oral dosing.

In-vitro vs systemic exposure relevance: Many in-vitro anticancer studies use low-to-mid micromolar concentrations, which are often difficult to reproduce reliably in vivo with unformulated parent betulinic acid. Accordingly, mechanistic findings are useful biologically, but direct concentration matching to standard oral/systemic use is often poor unless enhanced-delivery systems are used.

Clinical evidence status: Strong preclinical and formulation-development literature; very limited human oncology evidence. Cancer-facing clinical development appears to remain early-phase/topical, with orphan designation for topical metastatic melanoma but no FDA approval for that indication. Betulinic acid itself is not an established approved anticancer drug.

-half-life reports vary 3-5 hrs?. Reported half-life varies by formulation and species; several studies report multi-hour systemic persistence.
BioAv -hydrophobic molecule with relatively poor water solubility. 
Main Cancer action
-Direct mitochondrial targeting in cancer cells
-Minimal effect on normal cells

Key pathways
-Mitochondrial membrane permeabilization
-ROS-mediated apoptosis
-Caspase-independent death

Chemo relevance: Generally compatible, Not a redox buffer

Pathways:
- often induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells(Often associated with reduced redox buffering capacity in tumor cells (e.g., GSH depletion); NRF2 direction model-dependent.): NRF2↓, SOD↓, GSH↓
- May Raise AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑ Reports suggest relative sparing of normal cells and preservation of antioxidant capacity in some models
- lowers Inflammation : NF-kB↓(typ), COX2↓, p38↓ (context-dependent; often stress-activated), Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : , MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, VEGF↓, ROCK1↓, FAK↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : P53↑, HSP↓(model-dependent), Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓, EMT↓, TOP1↓,
- inhibits glycolysis (secondary to mitochondrial stress) ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, HK2↓, ECAR↓, GRP78↑(ER stress), GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, EGFR↓,
- inhibits Cancer Stem Cells in some studies : CSC↓, GLi1↓, β-catenin↓, OCT4↓,
- Others: PI3K↓(typ), AKT↓(typ), JAK↓, STAT↓, β-catenin↓, AMPK↓(AMPK is often activated during metabolic stress), ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,
- Selectivity: Cancer Cells vs Normal Cells

Mechanistic profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial permeabilization ↑ MOMP, ↓ ΔΨm, ↑ cytochrome c release, ↑ apoptosis ↔ / milder effect P-R Core tumor-selective death trigger Best-supported central mechanism; helps explain activity in apoptosis-competent but therapy-resistant tumors.
2 Mitochondrial ROS increase ↑ ROS ↔ / possible antioxidant sparing (context-dependent) P-R Amplifies mitochondrial stress and death signaling ROS appears mechanistically relevant in many tumor models, but not every study makes it the dominant initiating event.
3 Caspase axis and caspase-independent death ↑ caspase-9, ↑ caspase-3, ↑ PARP cleavage; caspase-independent death also reported ↔ R-G Executes apoptosis after mitochondrial injury BA can still kill some tumor cells when classical caspase execution is partly blocked, indicating non-canonical death contribution.
4 ER stress / UPR / GRP78 ↑ ER stress, ↑ UPR, ↑ GRP78 stress signaling ↔ R-G Links proteostatic stress to apoptosis and metastasis suppression Especially relevant in breast and gastric cancer models; may also connect to metabolic suppression and chemosensitization.
5 NF-κB survival signaling ↓ NF-κB ↔ / ↓ inflammatory tone R-G Reduces survival, inflammatory, and resistance programs Common downstream convergence node across several tumor types.
6 Cell-cycle machinery ↓ cyclin D1, ↓ CDK2, ↓ CDK4, ↑ cell-cycle arrest ↔ G Slows proliferation Usually supportive rather than primary; often follows stress and survival-pathway disruption.
7 EMT / invasion / matrix remodeling ↓ EMT, ↓ FAK, ↓ ROCK1, ↓ MMP2, ↓ MMP9, ↓ migration, ↓ invasion ↔ G Antimetastatic effect Consistent with reduced motility and invasive phenotype in multiple solid-tumor models.
8 Glycolysis ↓ glucose uptake, ↓ lactate, ↓ ECAR, ↓ HK2, ↓ PKM2, ↓ LDHA ↔ G Secondary metabolic suppression Not the universal initiating mechanism; appears important in selected breast-cancer and GRP78-linked systems.
9 HIF-1α hypoxia axis ↓ HIF-1α, ↓ VEGF, ↓ GLUT1, ↓ PDK1 ↔ G Reduces hypoxic adaptation and angiogenic drive Relevant in hypoxic tumor biology and helps explain antiangiogenic/metabolic effects in some models.
10 NRF2 / antioxidant buffering ↓ NRF2 or ↓ redox buffering (model-dependent) ↔ / possible preservation of antioxidant tone (context-dependent) R-G May widen tumor redox vulnerability Direction is not uniform across all models; safer to treat this as contextual rather than universally core.
11 Ca²⁺ stress ↑ Ca²⁺ (context-dependent) ↔ P-R Supports organelle stress and apoptotic signaling Usually part of the broader mitochondrial/ER stress network rather than a stand-alone primary target.
12 Radiosensitization or Chemosensitization ↑ sensitivity to radiation or selected drugs Unclear G Adjunct leverage Preclinical evidence supports additive or sensitizing effects with irradiation and with some chemotherapy settings, but this is not yet clinically established.
13 Clinical Translation Constraint Poor solubility and limited systemic exposure constrain reproducibility Same formulation constraint G Delivery bottleneck Main barrier is not lack of mechanistic richness but drug-like exposure; translation currently depends heavily on formulation, derivatization, or topical/local use.

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

  • P: 0–30 min (primary/physical-chemical effects; rapid kinase/redox signaling)
  • R: 30 min–3 hr (acute redox and stress-response activation)
  • G: >3 hr (gene-regulatory adaptation and phenotypic outcomes)
GRP78/BiP, HSPA5: Click to Expand ⟱
Source:
Type:
GRP78 (Pgp, BiP or ERp72) is a central regulator of endoplasmic reticulum (ER) function due to its roles in protein folding and assembly, targeting misfolded protein for degradation, ER Ca(2+)-binding and controlling the activation of trans-membrane ER stress sensors.
-GRP78 protein, a marker for endoplasmic reticulum stress
-GRP78’s role as a master regulator of the unfolded protein response (UPR) and cellular stress responses
The association of P-gp and inhibition of cell death in cancerous cells has also been reported in several studies including in hepatocellular, colorectal, prostate cancer, and gastric cancer. Although counterintuitive due to its prominent role in cancer resistance, P-gp has been linked to favorable prognosis.
ERp72 can promote cancer cell proliferation, migration, and invasion by regulating various signaling pathways, including the PI3K/AKT and MAPK/ERK pathways. Additionally, ERp72 can also inhibit apoptosis (programmed cell death) in cancer cells, which can contribute to tumor progression. Overexpressed in: Breast, lung colorectal, prostrate, ovarian, pancreatic.

-GRP78 is frequently upregulated in a variety of solid tumors and hematological malignancies.
-Overexpression of GRP78 in cancer cells is often regarded as a marker of increased ER stress due to the reduced oxygen and nutrient supply typically encountered in the tumor microenvironment.
-Elevated GRP78 levels can contribute to tumor cell survival by enhancing the adaptive UPR, allowing cancer cells to cope with therapeutic and metabolic stress.
Scientific Papers found: Click to Expand⟱
2763- BetA,    Betulinic Acid Inhibits the Stemness of Gastric Cancer Cells by Regulating the GRP78-TGF-β1 Signaling Pathway and Macrophage Polarization
- in-vitro, GC, NA
GRP78/BiP↓, The results indicated that BA inhibited not only GRP78-mediated stemness-related protein expression and GRP78-TGF-β-mediated macrophage polarization
TGF-β↓, BA Inhibits the Expression of GRP78, TGF-β1, and Stemness Markers in Human Gastric Cancer Cells
ChemoSen↑, BA is a promising candidate for clinical application in combination-chemotherapy targeting cancer stemness.
CSCs↓,
SMAD2↓, BA inhibited TGF-β/Smad2/3 signaling, TGF-β1 secretion, and OCT4 expression in a dose-dependent manner
SMAD3↓,
OCT4↓,

5591- BetA,    Advances and challenges in betulinic acid therapeutics and delivery systems for breast cancer prevention and treatment
- Review, BC, NA
BioAv↓, However, its poor water solubility limits its optimal therapeutic potential.
BioAv↑, nano-drug delivery systems (NDDSs) have gained significant attention as a method to substantially improve low solubility and poor drug bioavailability, enhance targeted drug delivery, and reduce side effects.
selectivity↑, reviews by Simone Fulda23,24 strengthened BA's potential for cancer treatment and prevention, particularly its ability to selectively trigger apoptosis in cancer cells while causing minimal harm to normal cells.
eff↑, It is important to note that the anticancer effects of BA on different types of tumors are more potent at a pH lower than 6.8.34
angioG↓, figure 3
*antiOx↑,
*Inflam↓,
MMP↓, BA-induced mitochondrial depolarization
Bcl-2↓, BA treatment has been shown to lower Bcl-2 expression and increase Bax, resulting in the activation of caspase-9 and caspase-3 through the mitochondrial pathway.63
BAX↑,
Casp9↑,
Casp3↑,
GRP78/BiP?, BA directly targets GRP78, triggering ER stress by activating the PERK-eIF2α-CHOP apoptotic cascade
ER Stress↑,
PERK↑,
CHOP↑,
ChemoSen↑, BA's ability to chemosensitize BC cells to taxanes highlights its importance in situations of drug resistance
SESN2↑, Under hypoxia, BA strongly increases SESN2 expression.
ROS↑, Reducing SESN2 levels enhances BA-induced ROS production, DNA damage, and radiosensitivity, while decreasing autophagic flux, indicating that SESN2-mediated autophagy serves as a protective adaptive response.68
MOMP↓, decreases the mitochondrial outer membrane potential (MOMP),
MAPK↑, This leads to the activation of p38 Mitogen-activated protein kinase (p38 MAPK), the release of cytochrome C, apoptosis-inducing factor (AIF),
Cyt‑c↑,
AIF↑,
STAT3↓, BA suppresses the signal transducer and activator of transcription (STAT) 3 signaling pathways
FAK↓, BA's inhibition of STAT3, as well as FAK, leads to decreased expression of MMPs and elevated TIMP-2, thereby impairing cancer cell migration and invasion
TIMP2↑,
TumCMig↓,
TumCI↓,
Sp1/3/4↓, Sp inhibition reduces cancer gene expression, inhibiting cancer cell growth.
TumCCA↑, It increases cell numbers in the G2/M phase, leading to cell cycle arrest.
DNAdam↑, causes DNA damage, thereby inhibiting the progression and invasion of cancer cells.

2720- BetA,    Betulinic acid induces apoptosis of HeLa cells via ROS-dependent ER stress and autophagy in vitro and in vivo
- in-vitro, Cerv, HeLa
Keap1↝, The findings revealed that BA activated Keap1/Nrf2 pathway and triggered mitochondria-dependent apoptosis due to ROS production.
ROS↑,
Ca+2↑, Furthermore, BA increased the intracellular Ca2+ levels
Beclin-1↓, inhibited the expression of Beclin1 and promoted the expression of GRP78, LC3-II, and p62 associated with ERS and autophagy.
GRP78/BiP↑,
LC3II↑,
p62↑,
ERStress↑,
TumAuto↑,

2729- BetA,    Betulinic acid in the treatment of tumour diseases: Application and research progress
- Review, Var, NA
ChemoSen↑, Betulinic acid can increase the sensitivity of cancer cells to other chemotherapy drugs
mt-ROS↑, BA has antitumour activity, and its mechanisms of action mainly include the induction of mitochondrial oxidative stress
STAT3↓, inhibition of signal transducer and activator of transcription 3 and nuclear factor-κB signalling pathways.
NF-kB↓,
selectivity↑, A main advantage of BA and its derivatives is that they are cytotoxic to different human tumour cells, while cytotoxicity is much lower in normal cells.
*toxicity↓, It can kill cancer cells but has no obvious effect on normal cells and is also nontoxic to other organs in xenograft mice at a dose of 500 mg/kg
eff↑, BA combined with chemotherapy drugs, such as platinum and mithramycin A, can induce apoptosis in tumour cells
GRP78/BiP↑, In animal xenograft tumour models, BA enhanced the expression of glucose-regulated protein 78 (GRP78)
MMP2↓, reduced the levels of matrix metalloproteinases (MMPs), such as MMP-2 and MMP-9, in lung metastatic lesions of breast cancer, indicating that BA can reduce the invasiveness of breast cancer in vivo and block epithelial mesenchymal transformation (EMT
P90RSK↓,
TumCI↓,
EMT↓,
MALAT1↓, MALAT1, a lncRNA, was downregulated in hepatocellular carcinoma (HCC) cells treated with BA in vivo,
Glycolysis↓, Suppressing aerobic glycolysis of cancer cells by GRP78/β-Catenin/c-Myc signalling pathways
AMPK↑, activating AMPK signaling pathway
Sp1/3/4↓, inhibiting Sp1. BA at 20 mg/kg/d, the tumour volume and weight were significantly reduced, and the expression levels of Sp1, Sp3, and Sp4 in tumour tissues were lower than those in control mouse tissues
Hif1a↓, Suppressing the hypoxia-induced accumulation of HIF-1α and expression of HIF target genes
angioG↓, PC3: Having anti-angiogenesis effect
NF-kB↑, LNCaP, DU145 — Inducing apoptosis and NF-κB pathway
NF-kB↓, U266 — Inhibiting NF-κB pathway.
MMP↓, BA produces ROS and reduces mitochondrial membrane potential; the mitochondrial permeability transition pore of the mitochondrial membrane plays an important role in apoptosis signal transduction.
Cyt‑c↑, Mitochondria release cytochrome C and increase the levels of Caspase-9 and Caspase-3, inducing cell apoptosis.
Casp9↑,
Casp3↑,
RadioS↑, BA could be a promising drug for increasing radiosensitization in oral squamous cell carcinoma radiotherapy.
PERK↑, BA treatment increased the activation of the protein kinase RNA-like endoplasmic reticulum kinase (PERK)/C/EBP homologous protein (CHOP) apoptosis pathway and decreased the expression of Sp1.
CHOP↑,
*toxicity↓, BA at a concentration of 50 μg/ml did not inhibit the growth of normal peripheral blood lymphocytes, indicating that the toxicity of BA was at least 1000 times less than that of doxorubicin

2738- BetA,    Betulinic Acid Suppresses Breast Cancer Metastasis by Targeting GRP78-Mediated Glycolysis and ER Stress Apoptotic Pathway
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vivo, NA, NA
TumCI↓, BA inhibited invasion and migration of highly aggressive breast cancer cells.
TumCMig↓,
Glycolysis↓, Moreover, BA could suppress aerobic glycolysis of breast cancer cells presenting as a reduction of lactate production, quiescent energy phenotype transition, and downregulation of aerobic glycolysis-related proteins.
lactateProd↓, lactate production in both MDA-MB-231 and BT-549 cells was significantly reduced following BA administration
GRP78/BiP↑, (GRP78) was also identified as the molecular target of BA in inhibiting aerobic glycolysis. BA treatment led to GRP78 overexpression, and GRP78 knockdown abrogated the inhibitory effect of BA on glycolysis.
ER Stress↑, Further studies demonstrated that overexpressed GRP78 activated the endoplasmic reticulum (ER) stress sensor PERK.
PERK↑,
p‑eIF2α↑, Subsequent phosphorylation of eIF2α led to the inhibition of β-catenin expression, which resulted in the inhibition of c-Myc-mediated glycolysis.
β-catenin/ZEB1↓,
cMyc↓, These findings suggested that BA inhibited the β-catenin/c-Myc pathway by interrupting the binding between GRP78 and PERK and ultimately suppressed the glycolysis of breast cancer cells.
ROS↑, (i) the induction of cancer cell apoptosis via the mitochondrial pathway induced by the release of soluble factors or generation of reactive oxygen species (ROS)
angioG↓, (ii) the inhibition of angiogenesis [24];
Sp1/3/4↓, (iii) the degradation of transcription factor specificity protein 1 (Sp1)
DNAdam↑, (iv) the induction of DNA damage by suppressing topoisomerase I
TOP1↓,
TumMeta↓, BA Inhibits Metastasis of Highly Aggressive Breast Cancer Cells
MMP2↓, BA significantly decreased the expression of MMP-2 and MMP-9 secreted by breast cancer cells
MMP9↓,
N-cadherin↓, BA downregulated the levels of N-cadherin and vimentin as the mesenchymal markers, while increased E-cadherin which is an epithelial marker (Figure 2(c)), validating the EMT inhibition effects of BA in breast cancer cells.
Vim↓,
E-cadherin↑,
EMT↓,
LDHA↓, the levels of glycolytic enzymes, including LDHA and p-PDK1/PDK1, were all decreased in a dose-dependent manner by BA
p‑PDK1↓,
PDK1↓,
ECAR↓, extracellular acidification rate (ECAR), which reflects the glycolysis activity, was retarded following BA administration.
OCR↓, oxygen consumption rate (OCR), which is a marker of mitochondrial respiration, was also decreased simultaneously
Hif1a↓, BA could reduce prostate cancer angiogenesis via inhibiting the HIF-1α/stat3 pathway [39]
STAT3↓,

2732- BetA,  Chemo,    Betulinic acid chemosensitizes breast cancer by triggering ER stress-mediated apoptosis by directly targeting GRP78
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
ChemoSen↑, Here in, we found that BA has synergistic effects with taxol to induce breast cancer cells G2/M checkpoint arrest and apoptosis induction,
selectivity↑, but had little cytotoxicity effects on normal mammary epithelial cells.
GRP78/BiP↑, identified glucose-regulated protein 78 (GRP78) as the direct interacting target of BA.
ER Stress↑, BA administration significantly elevated GRP78-mediated endoplasmic reticulum (ER) stress and resulted in the activation of protein kinase R-like ER kinase (PERK)/eukaryotic initiation factor 2a/CCAAT/enhancer-binding protein homologous protein apopt
PERK↑,
Ca+2↑, We found that BA significantly elevated intracellular free calcium concentration
Cyt‑c↑, increased Cytochrome c and Bax, and the downregulation of Bcl-2
BAX↑,
Bcl-2↓,


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Keap1↝, 1,   ROS↑, 3,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   MMP↓, 2,   OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   cMyc↓, 1,   ECAR↓, 1,   Glycolysis↓, 2,   lactateProd↓, 1,   LDHA↓, 1,   PDK1↓, 1,   p‑PDK1↓, 1,  

Cell Death ⓘ

BAX↑, 2,   Bcl-2↓, 2,   Casp3↑, 2,   Casp9↑, 2,   Cyt‑c↑, 3,   MAPK↑, 1,   MOMP↓, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 3,  

Protein Folding & ER Stress ⓘ

CHOP↑, 2,   p‑eIF2α↑, 1,   ER Stress↑, 3,   ERStress↑, 1,   GRP78/BiP?, 1,   GRP78/BiP↓, 1,   GRP78/BiP↑, 4,   PERK↑, 4,  

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1,   LC3II↑, 1,   p62↑, 1,   SESN2↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   EMT↓, 2,   OCT4↓, 1,   P90RSK↓, 1,   STAT3↓, 3,   TOP1↓, 1,  

Migration ⓘ

Ca+2↑, 2,   E-cadherin↑, 1,   FAK↓, 1,   MALAT1↓, 1,   MMP2↓, 2,   MMP9↓, 1,   N-cadherin↓, 1,   SMAD2↓, 1,   SMAD3↓, 1,   TGF-β↓, 1,   TIMP2↑, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumMeta↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   Hif1a↓, 2,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 2,   NF-kB↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 4,   eff↑, 2,   RadioS↑, 1,   selectivity↑, 3,  
Total Targets: 69

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

toxicity↓, 2,  
Total Targets: 3

Scientific Paper Hit Count for: GRP78/BiP, HSPA5
6 Betulinic acid
1 Chemotherapy
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#:42  Target#:356  State#:%  Dir#:%
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