Boswellia (frankincense) / NF-kB Cancer Research Results

Bos, Boswellia (frankincense): Click to Expand ⟱
Features:
Boswellia is an herbal extract from the Boswellia serrata tree that may help reduce inflammation.
May help with rheumatoid arthritis, inflammatory bowel disease, asthma, and cancer.
-Naturally occurring pentacyclic triterpenoids include ursolic acid (UA), oleanolic acid (OA), betulinic acid (BetA), bosewellic acid (BA), Asiatic acid (AA), α-amyrin, celastrol, glycyrrhizin, 18-β-glycyrrhetinic acid, lupeol, escin, madecassic acid, momordin I, platycodon D, pristimerin, saikosaponins, soyasapogenol B, and avicin
Boswellia refers to a group of resinous extracts obtained from Boswellia trees (e.g., Boswellia serrata). Traditionally used in Ayurvedic and traditional Chinese medicine, Boswellia is reputed for its anti-inflammatory, analgesic, and immunomodulatory properties. Its bioactive components—such as boswellic acids.
Boswellic acids belong to the pentacyclic triterpenoid class (a broader chemical family that includes compounds such as ursolic acid and betulinic acid found in other plants) 
      3-acetyl-11-keto-β-boswellic acid (AKBA) 
      11-keto-β-boswellic acid (KBA) 
      α-boswellic acid (αBA) 
      β-boswellic acid (βBA) 
      3-acetyl-α-boswellic acid (AαBA) 
      3-acetyl-β-boswellic acid (AβBA)
-Anti-inflammatory Activity (blocking the enzyme 5-lipoxygenase) 5LOX↓,.
-AKBA inhibits methionine adenosyltransferase 2A (MAT2A)***** (help in Methionine reduced diet?)
Boswellia extracts are often administered in doses ranging from 300 mg to 1,200 mg per day

AKBA (Acetyl-11-keto-β-boswellic acid) is a bioactive compound derived from Boswellia serrata, a plant used traditionally for its anti-inflammatory properties. (upto 30% AKBA in Boswellia MEGA AKBA)
AKBA also available in Inflasanum @ 90% AKDA (MCSformulas)

Boswellia (frankincense) — Boswellia refers to oleo-gum-resin extracts from Boswellia species, most commonly Boswellia serrata, enriched in pentacyclic triterpenes known as boswellic acids. It is best classified as a botanical extract / natural-product mixture rather than a single drug entity, although much of the mechanistic cancer literature focuses on specific constituents such as 3-acetyl-11-keto-β-boswellic acid (AKBA) and 11-keto-β-boswellic acid (KBA). Standard abbreviations include Bos, BS, BA, KBA, and AKBA. The dominant translational theme is anti-inflammatory and anti-edema activity with broader preclinical anticancer signaling effects; however, extract composition, formulation, and exposure vary substantially across studies.

Primary mechanisms (ranked):

  1. 5-lipoxygenase-linked leukotriene suppression and broader inflammatory eicosanoid downregulation
  2. NF-κB pathway suppression with downstream reduction of COX-2, cytokines, survival factors, and pro-metastatic genes
  3. Mitochondrial apoptosis and cell-cycle arrest in cancer models, including caspase activation, PARP cleavage, and cyclin/CDK suppression
  4. PI3K/Akt, ERK/MAPK, STAT3, Wnt/β-catenin, and related growth-signaling attenuation
  5. Anti-invasive / anti-angiogenic signaling, including MMP, VEGF, CXCR4, and EMT-related effects
  6. MAT2A inhibition by AKBA with one-carbon / SAM metabolism disruption
  7. Context-dependent redox modulation, with pro-apoptotic oxidative stress in some cancer models but antioxidant / NRF2-supportive effects reported in normal or inflamed tissues

Bioavailability / PK relevance: Boswellic acids are lipophilic and have poor oral bioavailability with marked formulation dependence. Human studies show food, especially a high-fat meal, substantially increases exposure, and reported half-life data are generally compatible with multi-hour persistence but not with reliably high systemic levels from standard extracts. Enhanced-delivery systems may improve exposure, but classic oral preparations remain PK-limited.

In-vitro vs systemic exposure relevance: Many mechanistic cancer studies use boswellic-acid concentrations in the roughly 10–50 µM range, which commonly exceed plasma exposure expected from standard oral Boswellia extracts. That makes direct translation of apoptosis, invasion, and signaling data uncertain unless high-exposure formulations, tissue accumulation, or local-compartment effects are demonstrated. Extract-level anti-inflammatory and edema effects are clinically more plausible than broad direct cytotoxic anticancer effects at routine oral dosing.

Clinical evidence status: Cancer-directed evidence remains limited. There is meaningful human evidence for adjunctive anti-edema use during/after brain tumor irradiation and a small phase Ia presurgical breast-cancer window study showing reduced proliferation markers, but there is no established oncologic approval and no robust phase III anticancer efficacy program. Overall status is preclinical-heavy with small human adjunct / early translational signals.


-Note half-life reports vary 2.5-90hrs?.
BioAv (bio availability increases with high fat meal)
Pathways:
- induce or lower ROS production (not consistant increase for cancer cells)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑,
- may Raise AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓">NF-kB↓, COX2↓, p38↓ (context-dependent; stress/inflammatory MAPK modulation), Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : , MMPs↓, MMP2↓, MMP9↓, VEGF↓, NF-κB↓, CXCR4↓, ERK↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, TOP1↓,
- inhibits angiogenesis↓ : VEGF↓, Notch↓, PDGF↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK(JNK is activated under stress)
- Synergies: chemo-sensitization, chemoProtective, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Hepatoprotective,

- Selectivity: Cancer Cells vs Normal Cells

Mechanistic profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 5-LOX eicosanoid signaling ↓ leukotriene-linked inflammatory drive ↓ inflammatory tone P, R Anti-inflammatory leverage Most historically grounded Boswellia mechanism; strongest at extract / boswellic-acid anti-inflammatory level and likely central to edema-control relevance.
2 NF-κB inflammatory survival axis ↓ NF-κB, COX-2, TNF-α, IL-1β, IL-6, VEGF, MMPs ↓ inflammatory stress R, G Anti-survival transcriptional suppression Supported across multiple tumor models; likely more translationally plausible as inflammation-modulating adjunct action than as stand-alone tumor cytotoxicity.
3 Mitochondrial apoptosis ↑ caspases, ↑ Cyt-c, ↓ MMP, ↑ cl-PARP ↔ / protective (context-dependent) R, G Programmed cell death Common in AKBA-focused in-vitro studies; robust mechanistically, but often demonstrated at concentrations that may exceed routine oral exposure.
4 Cell-cycle control ↓ cyclin D1, ↓ cyclin E, ↓ CDK2/4/6, ↑ arrest ↔ G Antiproliferative restraint Frequently accompanies apoptosis in colon, lung, breast, and hematologic models.
5 PI3K Akt ERK STAT growth signaling ↓ PI3K, ↓ Akt, ↓ ERK, ↓ STAT3 (context-dependent) ↔ / cytoprotective inflammatory dampening R, G Growth-signaling attenuation Plausible multi-target effect, but much of the literature is model-specific and extract-dependent.
6 EMT invasion angiogenesis axis ↓ EMT, ↓ MMP2/9, ↓ CXCR4, ↓ VEGF, ↓ migration / invasion ↔ G Anti-metastatic phenotype Consistent preclinical theme; clinically unproven as a direct antimetastatic therapy.
7 One-carbon metabolism MAT2A ↓ MAT2A activity (AKBA-specific), ↓ SAM flux (context-dependent) ↔ / uncertain R, G Metabolic / epigenetic stress Mechanistically important for AKBA, but direct evidence is strongest outside oncology; relevant as a credible target, not yet a clinically established Boswellia cancer mechanism.
8 Mitochondrial ROS increase ↑ ROS (context-dependent) ↓ ROS (context-dependent) R Redox bifurcation Cancer-cell oxidative push and normal-tissue antioxidant support can both appear in the literature; this is not a uniformly one-directional axis.
9 NRF2 antioxidant response ↔ / variable ↑ NRF2, ↑ SOD, ↑ GSH, ↑ catalase (context-dependent) G Normal-tissue cytoprotection More relevant for anti-inflammatory / tissue-protective use than for direct tumor kill; should be treated as secondary, not core, in cancer framing.
10 Chemosensitization or radiotherapy adjunct ↑ treatment response (context-dependent) ↑ edema control / possible steroid sparing G Adjunctive translational utility Human evidence is strongest for cerebral-edema reduction around brain tumor radiotherapy rather than for proven direct tumor response enhancement.
11 Clinical Translation Constraint Low systemic exposure from standard oral extracts Generally mild GI tolerability profile G PK-limited translation Poor solubility, food dependence, extract heterogeneity, and formulation variability are major reasons preclinical potency does not cleanly translate into established anticancer efficacy.

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

  • P: 0–30 min (primary/physical–chemical effects; rapid enzymatic/kinase shifts)
  • R: 30 min–3 hr (acute redox + stress-response signaling)
  • G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)
NF-kB, Nuclear factor kappa B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
NF-kB signaling
Nuclear factor kappa B (NF-κB) is a transcription factor that plays a crucial role in regulating immune response, inflammation, cell proliferation, and survival.
NF-κB is often found to be constitutively active in many types of cancer cells. This persistent activation can promote tumorigenesis by enhancing cell survival, proliferation, and metastasis.
Scientific Papers found: Click to Expand⟱
2777- Bos,    Boswellia serrata Preserves Intestinal Epithelial Barrier from Oxidative and Inflammatory Damage
- in-vitro, IBD, NA
*p‑NF-kB↓, BSE and AKBA pretreatment significantly prevented functional and morphological alterations and also the NF-κB phosphorylation induced by the inflammatory stimuli.
*ROS↓, At the same concentrations BSE and AKBA counteracted the increase of ROS caused by H2O2 exposure.
Inflam↓, BSE, in protecting intestinal epithelial barrier from inflammatory damage and supports its use as safe adjuvant in patients affected by IBD.

2767- Bos,    The potential role of boswellic acids in cancer prevention and treatment
- Review, Var, NA
*Inflam↓, profound application as a traditional remedy for various ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer
AntiCan↑,
*MAPK↑, 11-keto-BAs can stimulate Mitogen-activated protein kinases (MAPK) and mobilize the intracellular Ca(2+) that are important for the activation of human polymorphonuclear leucocytes (PMNL)
*Ca+2↝,
p‑ERK↓, AKBA prohibited the phosphorylation of extracellular signal-regulated kinase-1 and -2 (Erk-1/2) and impaired the motility of meningioma cells stimulated with platelet-derived growth factor BB
TumCI↓,
cycD1/CCND1↓, In the case of colon cancer, BA treatment on HCT-116 cells led to a decrease in cyclin D, cyclin E, and Cyclin-dependent kinases such as CDK2 and CDK4, along with significant reduction in phosphorylated Rb (pRb)
cycE/CCNE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
*NF-kB↓, convey inhibition of NF-kappaB and subsequent down-regulation of TNF-alpha expression in activated human monocytes
*TNF-α↓,
NF-kB↓, PC-3 prostate cancer cells in vitro and in vivo by inhibiting constitutively activated NF-kappaB signaling by intercepting the activity of IkappaB kinase (IKK
IKKα↓,
MCP1↓, LPS-challenged ApoE-/- mice via inhibition of NF-κB and down regulation of MCP-1, MCP-3, IL-1alpha, MIP-2, VEGF, and TF
IL1α↓,
MIP2↓,
VEGF↓,
Tf↓,
COX2↓, pancreatic cancer cell lines, AKBA inhibited the constitutive expression of NF-kB and caused suppression of NF-kB regulated genes such as COX-2, MMP-9, CXCR4, and VEGF
MMP9↓,
CXCR4↓,
VEGF↓,
eff↑, AKBA and aspirin revealed that AKBA has higher potential via modulation of the Wnt/β-catenin pathway, and NF-kB/COX-2 pathway in adenomatous polyps
PPARα↓, AKBA is also responsible for down-regulation of PPAR-alpha and C/EBP-alpha in a dose and temporal dependent manner in mature adipocytes, ultimately leading to pparlipolysis
lipid-P?,
STAT3↓, activation of STAT-3 in human MM cells could be inhibited by AKBA
TOP1↓, (PKBA; a semisynthetic analogue of 11-keto-β-boswellic acid), had been reported to influence the activity of topoisomerase I & II,
TOP2↑,
5HT↓, (5-LO), responsible for catalyzing the synthesis of leukotrienes from arachidonic acid and human leucocyte elastase (HLE), and serine proteases involved in several inflammatory processes, is considered to be a potent molecular target of BA derivative
p‑PDGFR-BB↓, BA up-regulates SHP-1 with subsequent dephosphorylation of PDGFR-β and downregulation of PDGF-dependent signaling after PDGF stimulation, thereby exerting an anti-proliferative effect on HSCs hepatic stellate cells
PDGF↓,
AR↓, AKBA targets different receptors that include androgen receptor (AR), death receptor 5 (DR5), and vascular endothelial growth factor receptor 2 (VEGFR2), and leads to the inhibition of proliferation of prostate cancer cells
DR5↑, induced expression of DR4 and DR5.
angioG↓, via apoptosis induction and suppression of angiogenesis
DR4↑,
Casp3↑, AKBA resulted in activation of caspase-3 and caspase-8, and initiation of poly (ADP) ribose polymerase (PARP) cleavage.
Casp8↑,
cl‑PARP↑,
eff↑, AKBA was preincubated with LY294002 or wortmannin (inhibitors of PI3K), it caused a significant enhancement of apoptosis in HT-29 cells
chemoPv↑, chemopreventive response of AKBA was estimated against intestinal adenomatous polyposis through the inhibition of the Wnt/β-catenin and NF-κB/cyclooxygenase-2 signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
ascitic↓, AKBA by the suppression of ascites,
Let-7↑, AKBA could up-regulate the expression of let-7 and miR-200
miR-200b↑,
eff↑, anti-tumorigenic effects of curcumin and AKBA on the regulation of specific cancer-related miRNAs in colorectal cancer cells, and confirmed their protective action
MMP1↓, . It can inhibit the expression of MMP-1, MMP-2, and MMP-9 mRNAs along with secretions of TNF-α and IL-1β in THP-1 cells.
MMP2↓,
eff↑, combined administration of metformin, an anti-diabetic drug, and boswellic acid nanoparticles exhibited significant synergism through the inhibition of MiaPaCa-2 pancreatic cancer cell proliferation
BioAv↓, BA as a therapeutic drug is its poor bioavailability
BioAv↑, administration of BSE-018 concomitantly with a high-fat meal led to several-fold increased areas under the plasma concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA)
Half-Life↓, drug needs to be given orally at the interval of six hours due to its calculated half- life, which was around 6 hrs.
toxicity↓, BSE has been found to be a safe drug without any adverse side reactions, and is well tolerated on oral administration.
Dose↑, Boswellia serrata extract to the maximum amount of 4200 mg/day is not toxic and it is safe to use though it shows poor bioavailability
BioAv↑, Approaches like lecithin delivery form (Phytosome®), nanoparticle delivery systems like liposomes, emulsions, solid lipid nanoparticles, nanostructured lipid carriers, micelles and poly (lactic-co-glycolic acid) nanoparticles
ChemoSen↑, Like any other natural products BA can also be effective as chemosensitizer

2768- Bos,    Boswellic acids as promising agents for the management of brain diseases
- Review, Var, NA - Review, AD, NA - Review, Park, NA
*neuroP↑, BAs-induced neuroprotection is proposed to be associated with the ability to reduce neurotoxic aggregates, decrease oxidative stress, and improve cognitive dysfunction.
*ROS↓,
*cognitive↓,
TumCP↓, BAs have been suggested as potential agents for the treatment of brain tumors due to their potential to attenuate cell proliferation, migration, metastasis, angiogenesis, and promote apoptosis during both in vitro and in vivo studies
TumCMig↓,
TumMeta↓,
angioG↓,
Apoptosis↑,
*Inflam↓, The anti-inflammatory activities of BAs have been investigated in many preclinical and clinical trials
IL1↓, BAs inhibit the production of pro-inflammatory cytokines such as interleukin-1 (IL-1), IL-2, IL-4, IL-6, and tumor necrosis factor-α (TNF-α) in several experimental studies.
IL2↓,
IL4↓,
IL6↓,
TNF-α↓,
P53↑, AKBA has been reported to induce apoptosis in pancreatic and gastric cancers, through tumor suppressor protein 53 (p53)-independent pathway, while reducing expression of protein kinase (PK) B and NF-kb
Akt↓,
NF-kB↓,
DNAdam↑, DNA fragmentation, and activation of caspase cascade
Casp↑,
COX2↓, regulated genes such as cyclooxygenase-2 (COX-2), matrix metallopeptidase-9 (MMP-9), C-X-C motif chemokine receptor 4 (CXCR4), and vascular endothelial growth factor (VEGF)
MMP9↓,
CXCR4↓,
VEGF↓,
*SOD↑, BAs against oxidative injury has been shown in several cell lines and animal models [12], [13], [21]. BAs exert protective effects through the normalization of antioxidant enzyme levels, such as superoxide dismutase (SOD), catalase, and glutathione p
*Catalase↑,
*GPx↑,
*NRF2↑, Moreover, it can activate nuclear factor erythroid 2-related factor-2 (Nrf2)/antioxidant response element-regulated pathways

2772- Bos,    Mechanistic role of boswellic acids in Alzheimer’s disease: Emphasis on anti-inflammatory properties
- Review, AD, NA
*neuroP↑, (AKBA) that possess potent anti-inflammatory and neuroprotective properties in AD
*Inflam↓,
*AChE↓, inhibiting the acetylcholinesterase (AChE) activity in the cholinergic pathway and improve choline levels
*Choline↑,
*NRF2↑, BAs modulate key molecular targets and signalling pathways like 5-lipoxygenase/cyclooxygenase, Nrf2, NF-kB, cholinergic, amyloid-beta (Aβ), and neurofibrillary tangles formation (NFTs) that are involved in AD
*NF-kB↑,
*BBB↑, AKBA has efficiently abled to cross the blood brain barrier (BBB)
*BioAv↑, bioavailability of AKBA was significantly higher in case of sublingual route when compared to intranasal administration, as demonstrated by area under curves (AUCs) analysis
*Half-Life↓, half-life of the drug was about six hours and peak plasma levels of the drug reach 30 hrs after oral administration of 333 mg of BSE.
*Dose↝, drug needs to be administered at a dosing interval of 6 hrs
*PGE2↓, BAs possessed anti-inflammatory activity by inhibiting microsomal prostaglandin E2 synthase-1 (mPGES1)
*ROS↓, prevented oxidative stress-induced neuronal damage and cognitive impairment because of the antioxidant, anti-inflammatory and anti-glutamatergic effects
*cognitive↑,
*antiOx↑,
5LO↓, AKBA significantly reduced pro-inflammatory mediators such as 5-LOX, TNF-α, IL-6 levels and improve cognition
*TNF-α↓,
*IL6↓,
*HO-1↑, AKBA shows neuroprotective effects against ischaemic injury via nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) cascade activation

2773- Bos,    Targeted inhibition of tumor proliferation, survival, and metastasis by pentacyclic triterpenoids: Potential role in prevention and therapy of cancer
- Review, Var, NA
Inflam↓, BA has been shown to be effective against chronic inflammation-driven diseases such as adjuvant or bovine serum albumin-induced arthritis, osteoarthritis, Crohn’s disease, ulcerative colitis, and ileitis, and galactosamine/endotoxin-induced hepa
TumCCA↑, BA induced apoptosis was mediated by cell cycle arrest in the G1 phase and by activating caspases 3, 8 and 9 in HT-29 cells
Casp3↑,
Casp8↑,
Casp9↑,
STAT3↑, BA inhibited the growth of multiple myeloma cells by suppression of STAT3 pathway and by activation of protein tyrosine phosphatase SHP1
SHP1↓,
NF-kB↓, BA down regulated the expression of NF-kB, cyclin D1, COX2, Ki-67, CD-31 and IAPs in the tumor tissue.
cycD1/CCND1↓,
COX2↓,
Ki-67↓,
CD31↓,
IAP1↓,
MMPs↓, AKBA induced cell cycle arrest was mediated by down-regulating the expression of cyclinD1, suppresses MMP activity, and also induced apoptosis by suppressing Bcl-2, and Bcl-xL expression
Bcl-2↓,
Bcl-xL↓,

2774- Bos,    Boswellia ovalifoliolata abrogates ROS mediated NF-κB activation, causes apoptosis and chemosensitization in Triple Negative Breast Cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-453
ChemoSen↑, BL EthOH has synergistic chemosensitizing effects on TNBC cells and increased the cytotoxicity of doxorubicin and cisplatin
Casp3↑, BL EthOH caused 5 folds and 6 folds increase of caspase 3 levels in both MDA-MB-231 and MDA-MB-453 cells respectively when compared with the untreated control cells
ROS↓, treatment with plant extract significantly inhibited the H 2 O2 induced ROS generation in both MDA-MB-231 and MDA-MB-453 cells.
NF-kB↓, The expression of phospho-NF-kB (ser536) decreased dose dependently in MDA-MB-231and MDA-MB-453cells after treatment with BL EthOH.

2775- Bos,    The journey of boswellic acids from synthesis to pharmacological activities
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
ROS↑, modulation of reactive oxygen species (ROS) formation and the resulting endoplasmic reticulum stress is central to BA’s molecular and cellular anticancer activities
ER Stress↑,
TumCG↓, Cell cycle arrest, growth inhibition, apoptosis induction, and control of inflammation are all the effects of BA’s altered gene expression
Apoptosis↑,
Inflam↓,
ChemoSen↑, BA has additional synergistic effects, increasing both the sensitivity and cytotoxicity of doxorubicin and cisplatin
Casp↑, BA decreases viability and induces apoptosis by activat- ing the caspase-dependent pathway in human pancreatic cancer (PC) cell lines
ERK↓, BA might inhibit the activation of Ak strain transforming (Akt) and extracellular signal–regulated kinase (ERK)1/2,
cl‑PARP↑, initiation of cleavage of PARP were prompted by the treatment with AKBA
AR↓, AKBA affects the androgen receptor by reducing its expression,
cycD1/CCND1↓, decrease in cyclin D1, which inhibits cellular proliferation
VEGFR2↓, In prostate cancer, the downregulation of vascular endothelial growth factor receptor 2–mediated angiogenesis caused by BA
CXCR4↓, Figure 6
radioP↑,
NF-kB↓,
VEGF↓,
P21↑,
Wnt↓,
β-catenin/ZEB1↓,
Cyt‑c↑,
MMP2↓,
MMP1↓,
MMP9↓,
PI3K↓,
MAPK↓,
JNK↑,
*5LO↓, Table 1 (non cancer)
*NRF2↑,
*HO-1↑,
*MDA↓,
*SOD↑,
*hepatoP↑, Preclinical studies demonstrated hepatoprotective impact for BA against different models of hepatotoxicity via tackling oxidative stress, and inflammatory and apoptotic indices
*ALAT↓,
*AST↓,
*LDH↑,
*CRP↓,
*COX2↓,
*GSH↑,
*ROS↓,
*Imm↑, oral administration of biopolymeric fraction (BOS 200) from B. serrata in mice led to immunostimulatory effects
*Dose↝, BA at low concentration tend to stimulate an immune response, as those utilized in the study of Beghelli et al. (2017) however, utilizing higher concentration suppressed the immune response
*eff↑, Useful actions on skin and psoriasis
*neuroP↑, AKBA has substantially diminished the levels of inflammatory markers such as 5-LOX, TNF-, IL-6, and meliorated cognition in lipopolysaccharide-induced neuroinflammation rodent models
*cognitive↑,
*IL6↓,
*TNF-α↓,

3866- Bos,    Mechanistic role of boswellic acids in Alzheimer's disease: Emphasis on anti-inflammatory properties
- Review, AD, NA
*neuroP↑, therapeutic potential against multiple neurodegenerative diseases such as Alzheimer's disease (AD).
*Inflam↓, main chemical constituents of this gum include boswellic acids (BAs) like 3-O-acetyl-11-keto-β boswellic acid (AKBA) that possess potent anti-inflammatory and neuroprotective properties in AD
*AChE↓, It is also involved in inhibiting the acetylcholinesterase (AChE) activity in the cholinergic pathway and improve choline levels
*Ach↑,
*NRF2↑, activating Nrf2 through binding of ARE, inhibiting NF-kB and AChE activity.
*NF-kB↓,
*Aβ↓, inhibition of amyloid plaques (Aβ) and neurofibrillary tangles (NFTs) induced neurotoxicity and neuroinflammation in AD

1423- Bos,    Acetyl-11-keto-β-Boswellic Acid Suppresses Invasion of Pancreatic Cancer Cells Through The Downregulation of CXCR4 Chemokine Receptor Expression
- in-vitro, Melanoma, U266 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, SkBr3 - in-vitro, PC, PANC1
CXCR4↓, AKBA is a novel inhibitor of CXCR4 expression
TumCI↓,
HER2/EBBR2↓, AKBA downregulated the expression of HER2 in all pancreatic cancer cells, but not in all breast cancer cell lines.
NF-kB↓,

1185- Bos,    The journey of boswellic acids from synthesis to pharmacological activities
- Review, NA, NA
BAX↑,
NF-kB↓,
cl‑PARP↑,
Casp3↑,
Casp8↑,

1416- Bos,    Anti-cancer properties of boswellic acids: mechanism of action as anti-cancerous agent
- Review, NA, NA
5LO↓,
TumCCA↑, G0/G1 phase
LC3B↓, reduced the expression of LC3A/B-I and LC3A/B-II,
PI3K↓,
Akt↓,
Glycolysis↓,
AMPK↑,
mTOR↓,
Let-7↑,
COX2↓, methanolic extract decreased the expression of cyclooxygenase-2 gene
VEGF↓,
CXCR4↓,
MMP2↓,
MMP9↓,
HIF-1↓,
angioG↓,
TumCP↓,
TumCMig↓,
NF-kB↓,

1422- Bos,    Boswellic acid exerts antitumor effects in colorectal cancer cells by modulating expression of the let-7 and miR-200 microRNA family
- in-vitro, CRC, NA - in-vivo, NA, NA
5LO↓, boswellic acids, is known to be a non-redox and non-competitive inhibitor of 5-lipoxygenase
TumCG↓,
Let-7↑,
miR-200b↑, AKBA significantly up-regulated expression of the let-7 and miR-200 families in various CRC cell lines
NF-kB↓,
cMyc↓,
cycD1/CCND1↓,
MMP9↓,
CXCR4↓,
VEGF↓,
Bcl-xL↓,
survivin↓,
IAP1↓,
XIAP↓,
TumCG↓,
CDK6↓,
Vim↓,
E-cadherin↑,

1169- Bos,    Boswellic Acid Inhibits Growth and Metastasis of Human Colorectal Cancer in Orthotopic Mouse Model By Downregulating Inflammatory, Proliferative, Invasive, and Angiogenic Biomarkers
- in-vivo, CRC, NA
TumCG↓,
TumVol↓,
Weight∅, without significant decreases in body weight
ascitic↓,
TumMeta↓,
Ki-67↓,
CD31↓,
NF-kB↓,
COX2↓,
Bcl-2↓,
Bcl-xL↓,
IAP1↓,
survivin↓,
cycD1/CCND1↓,
ICAM-1↓,
MMP9↓,
CXCR4↓,
VEGF↓,


Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

lipid-P?, 1,   ROS↓, 1,   ROS↑, 1,  

Metal & Cofactor Biology ⓘ

Tf↓, 1,  

Mitochondria & Bioenergetics ⓘ

XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   cMyc↓, 1,   Glycolysis↓, 1,   PPARα↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 2,   Bcl-xL↓, 3,   Casp↑, 2,   Casp3↑, 4,   Casp8↑, 3,   Casp9↑, 1,   Cyt‑c↑, 1,   DR4↑, 1,   DR5↑, 1,   IAP1↓, 3,   JNK↑, 1,   MAPK↓, 1,   survivin↓, 2,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

LC3B↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,   cl‑PARP↑, 3,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 5,   cycE/CCNE↓, 1,   P21↑, 1,   p‑RB1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   p‑ERK↓, 1,   Let-7↑, 3,   mTOR↓, 1,   PI3K↓, 2,   SHP1↓, 1,   STAT3↓, 1,   STAT3↑, 1,   TOP1↓, 1,   TOP2↑, 1,   TumCG↓, 4,   Wnt↓, 2,  

Migration ⓘ

5LO↓, 3,   CD31↓, 2,   E-cadherin↑, 1,   Ki-67↓, 2,   miR-200b↑, 2,   MMP1↓, 2,   MMP2↓, 3,   MMP9↓, 6,   MMPs↓, 1,   PDGF↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 2,   TumMeta↓, 2,   Vim↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   HIF-1↓, 1,   p‑PDGFR-BB↓, 1,   VEGF↓, 7,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 5,   CXCR4↓, 7,   ICAM-1↓, 1,   IKKα↓, 1,   IL1↓, 1,   IL1α↓, 1,   IL2↓, 1,   IL4↓, 1,   IL6↓, 1,   Inflam↓, 3,   MCP1↓, 1,   MIP2↓, 1,   NF-kB↓, 10,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 2,   CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   ChemoSen↑, 3,   Dose↑, 1,   eff↑, 4,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

AR↓, 2,   ascitic↓, 2,   HER2/EBBR2↓, 1,   IL6↓, 1,   Ki-67↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoPv↑, 1,   radioP↑, 1,   toxicity↓, 1,   TumVol↓, 1,   Weight∅, 1,  
Total Targets: 105

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   HO-1↑, 2,   MDA↓, 1,   NRF2↑, 4,   ROS↓, 4,   SOD↑, 2,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   LDH↑, 1,  

Cell Death ⓘ

MAPK↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Choline↑, 1,  

Migration ⓘ

5LO↓, 1,   Ca+2↝, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CRP↓, 1,   IL6↓, 2,   Imm↑, 1,   Inflam↓, 4,   NF-kB↓, 2,   NF-kB↑, 1,   p‑NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 3,  

Synaptic & Neurotransmission ⓘ

AChE↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   Dose↝, 2,   eff↑, 1,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   CRP↓, 1,   IL6↓, 2,   LDH↑, 1,  

Functional Outcomes ⓘ

cognitive↓, 1,   cognitive↑, 2,   hepatoP↑, 1,   neuroP↑, 4,  
Total Targets: 42

Scientific Paper Hit Count for: NF-kB, Nuclear factor kappa B
13 Boswellia (frankincense)
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#:47  Target#:214  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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