Database Query Results : Boswellia (frankincense), , AMPK

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)

-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↓, 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

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 NF-κB axis (IKK → NF-κB; NF-κB-regulated genes) NF-κB ↓; downstream targets ↓ (COX-2, Cyclin D1, Bcl-2/Bcl-xL/IAPs, MMP-9, VEGF, CXCR4 etc.) Anti-inflammatory tone (context) R, G Anti-survival / anti-inflammatory transcription AKBA-class compounds suppress NF-κB signaling and reduce multiple NF-κB-regulated tumor programs in vitro and in vivo models.
2 5-LOX (leukotriene pathway) / eicosanoid signaling 5-LOX activity ↓ (context); pro-inflammatory eicosanoid signaling ↓ Anti-inflammatory support P, R Direct enzymatic / lipid-mediator suppression Boswellic acids are widely discussed as 5-LOX–linked anti-inflammatory agents; cancer relevance often tracks inflammation-driven growth signals.
3 Apoptosis (extrinsic + intrinsic; caspases; PARP) Apoptosis ↑; Caspase-8/3 ↑; cl-PARP ↑ (context) ↔ G Cell death execution Reported apoptosis induction includes death-receptor (e.g., DR5-associated) and caspase/PARP cleavage patterns in multiple tumor models.
4 Cell-cycle control (Cyclin D1 / checkpoints) Cyclin D1 ↓; proliferation ↓; arrest ↑ (context) ↔ G Cytostasis Often presented as downstream of NF-κB/survival signaling suppression and stress adaptation.
5 Invasion / metastasis programs (MMP-9, ICAM-1, CXCR4) Invasion markers ↓; MMP-9 ↓; ICAM-1 ↓; CXCR4 ↓ (context) ↔ G Anti-invasive phenotype In vivo tumor models report reductions in invasive and chemokine/migration biomarkers alongside NF-κB suppression.
6 Angiogenesis signaling (VEGF; VEGFR2-mediated angiogenesis) VEGF ↓; angiogenic outputs ↓ (context) ↔ G Anti-angiogenic support AKBA has been reported to suppress angiogenesis programs including VEGF signaling, with VEGFR2-mediated angiogenesis discussed in prostate cancer contexts.
7 PI3K → AKT (± mTOR) survival axis PI3K/AKT ↓ (reported; model-dependent) ↔ R, G Growth/survival suppression Commonly listed as a downstream survival pathway impacted by boswellic acids; keep as “reported” (not universal across all models).
8 MAPK re-wiring (ERK / JNK / p38) Stress-MAPK modulation (context-dependent) ↔ P, R, G Signal reprogramming MAPK direction varies by tumor type/dose and whether the experimental system is inflammatory vs cytotoxic.
9 Chemo-/radio-sensitization (combination relevance) Sensitization ↑ (context) — G Combination leverage Combination studies report enhanced tumor control when AKBA-class compounds are paired with other therapies (context and regimen dependent).
10 Bioavailability constraint (oral exposure; formulation dependence) Systemic exposure often limited without enhanced delivery — — Translation constraint Poor pharmacokinetics are a common limitation; multiple strategies (e.g., micellar delivery, bioenhancers) are studied to improve absorption.

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)
AMPK, adenosine monophosphate-activated protein kinase: Click to Expand ⟱
Source:
Type:
AMPK: guardian of metabolism and mitochondrial homeostasis; Upon changes in the ATP-to-AMP ratio, AMPK is activated. (AMPK) is a key metabolic sensor that is pivotal for the maintenance of cellular energy homeostasis. It is well documented that AMPK possesses a suppressor role in the context of tumor development and progression by modulating the inflammatory and metabolic pathways.

-Activating AMPK can inhibit anabolic processes and the PI3K/Akt/mTOR pathway reducing glycolysis shifting toward Oxidative Phosphorlylation.


AMPK activators:
-metformin or AICAR
-Resveratrol: activate AMPK indirectly
-Berberine
-Quercetin: may stimulate AMPK
-EGCG: thought to activate AMPK
-Curcumin: may activate AMPK

-Ginsenosides: Some ginsenosides have been associated with AMPK activation -Beta-Lapachone: A natural naphthoquinone compound found in the bark of Tabebuia avellanedae (also known as lapacho or taheebo). It has been observed to activate AMPK in certain models.
-Alpha-Lipoic Acid (ALA): associated with AMPK activation
Scientific Papers found: Click to Expand⟱
2776- Bos,    Anti-inflammatory and anti-cancer activities of frankincense: Targets, treatments and toxicities
- Review, Var, NA
*5LO↓, Arthritis Human primary chondrocytes: 5-LOX↓, TNF-α↓, MMP3↓
*TNF-α↓,
*MMP3↓,
*COX1↓, COX-1↓, Leukotriene synthesis by 5-LOX↓
*COX2↓, Arthritis Human blood in vitro: COX-2↓, PGE2↓, TH1 cytokines↓, TH2 cytokines↑
*PGE2↓,
*Th2↑,
*Catalase↑, Ethanol-induced gastric ulcer: CAT↑, SOD↑, NO↑, PGE-2↑
*SOD↑,
*NO↑,
*PGE2↑,
*IL1β↓, inflammation Human PBMC, murine RAW264.7 macrophages: TNFα↓ IL-1β↓, IL-6↓, Th1 cytokines (IFNγ, IL-12)↓, Th2 cytokines (IL-4, IL-10)↑; iNOS↓, NO↓, phosphorylation of JNK and p38↓
*IL6↓,
*Th1 response↓,
*Th2↑,
*iNOS↓,
*NO↓,
*p‑JNK↓,
*p38↓,
GutMicro↑, colon carcinogenesis: gut microbiota; pAKT↓, GSK3β↓, cyclin D1↓
p‑Akt↓,
GSK‐3β↓,
cycD1/CCND1↓,
Akt↓, Prostate Ca: AKT and STAT3↓, stemness markers↓, androgen receptor↓, Sp1 promoter binding↓, p21(WAF1/CIP1)↑, cyclin D1↓, cyclin D2↓, DR5↑,CHOP↑, caspases-3/-8↑, PARP cleavage, NFκB↓, IKK↓, Bcl-2↓, Bcl-xL↓, caspase 3↑, DNA
STAT3↓,
CSCs↓,
AR↓,
P21↑,
DR5↑,
CHOP↑,
Casp3↑,
Casp8↑,
cl‑PARP↑,
DNAdam↑,
p‑RB1↓, Glioblastoma: pRB↓, FOXM1↓, PLK1↓, Aurora B/TOP2A pathway↓,CDC25C↓, pCDK1↓, cyclinB1↓, Aurora B↓, TOP2A↓, pERK-1/-2↓
FOXM1↓,
TOP2↓,
CDC25↓,
p‑CDK1↓,
p‑ERK↓,
MMP9↓, Pancreas Ca: Ki-67↓, CD31↓, COX-2↓, MMP-9↓, CXCR4↓, VEGF↓
VEGF↓,
angioG↓, Apoptosis↑, G2/M arrest, angiogenesis↓
ROS↑, ROS↑,
Cyt‑c↑, Leukemia : cytochrome c↑, AIF↑, SMAC/DIABLO↑, survivin↓, ICAD↓
AIF↑,
Diablo↑,
survivin↓,
ICAD↓,
ChemoSen↑, Breast Ca: enhancement in combination with doxorubicin
SOX9↓, SOX9↓
ER Stress↑, Cervix Ca : ER-stress protein GRP78↑, CHOP↑, calpain↑
GRP78/BiP↑,
cal2↓,
AMPK↓, Breast Ca: AMPK/mTOR signaling↓
mTOR↓,
ROS↓, Boswellia extracts and its phytochemicals reduced oxidative stress (in terms of inhibition of ROS and RNS generation)

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↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   CDC25↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↓, 1,   AMPK↑, 1,   Glycolysis↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Cyt‑c↑, 1,   Diablo↑, 1,   DR5↑, 1,   ICAD↓, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

SOX9↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,  

Autophagy & Lysosomes ⓘ

LC3B↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

p‑CDK1↓, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   p‑RB1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   p‑ERK↓, 1,   FOXM1↓, 1,   GSK‐3β↓, 1,   Let-7↑, 1,   mTOR↓, 2,   PI3K↓, 1,   STAT3↓, 1,   TOP2↓, 1,  

Migration ⓘ

5LO↓, 1,   cal2↓, 1,   MMP2↓, 1,   MMP9↓, 2,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   HIF-1↓, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CXCR4↓, 1,   NF-kB↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   FOXM1↓, 1,   GutMicro↑, 1,  
Total Targets: 54

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   SOD↑, 1,  

Cell Death ⓘ

iNOS↓, 1,   p‑JNK↓, 1,   p38↓, 1,  

Migration ⓘ

5LO↓, 1,   MMP3↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,   NO↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX1↓, 1,   COX2↓, 1,   IL1β↓, 1,   IL6↓, 1,   PGE2↓, 1,   PGE2↑, 1,   Th1 response↓, 1,   Th2↑, 2,   TNF-α↓, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  
Total Targets: 19

Scientific Paper Hit Count for: AMPK, adenosine monophosphate-activated protein kinase
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#:9  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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