Database Query Results : Boswellia (frankincense), , MMPs

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)
MMPs, Matrix metalloproteinases: Click to Expand ⟱
Source:
Type:
Family of zinc-dependent proteolytic enzymes that play a key role in degrading the extracellular matrix (ECM).; are metalloproteinases that are calcium-dependent zinc-containing endopeptidases;[1] other family members are adamalysins, serralysins, and astacins. The MMPs belong to a larger family of proteases known as the metzincin superfamily.[2]
MMP secretion: matrix metalloproteinase (MMP) is a kind of enzymes secreted.
by tumor cell to degrade ECM, facilitating the migration of tumor cells.

MMPs are generally considered protumorigenic due to their role in promoting tumor invasion, metastasis, and angiogenesis. They facilitate the breakdown of the extracellular matrix, allowing cancer cells to invade surrounding tissues and spread to distant sites.
Scientific Papers found: Click to Expand⟱
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↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   IAP1↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

SHP1↓, 1,   STAT3↑, 1,  

Migration ⓘ

CD31↓, 1,   Ki-67↓, 1,   MMPs↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 1,   NF-kB↓, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,  
Total Targets: 17

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: MMPs, Matrix metalloproteinases
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#:204  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

Home Page