tbResList Print — Bos Boswellia (frankincense)

Description: <b>Boswellia</b> is an herbal extract from the Boswellia serrata tree that may help reduce inflammation.<br>
May help with rheumatoid arthritis, inflammatory bowel disease, asthma, and cancer.<br>
-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<br>
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.<br>
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)
<pre>
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)
</pre>
-Anti-inflammatory Activity (blocking the enzyme 5-lipoxygenase)
<a href="tbResList.php?qv=47&tsv=1090&wNotes=on">5LOX↓</a>,.<br>
-AKBA inhibits
<a href="tbResList.php?qv=47&tsv=1206&wNotes=on">methionine adenosyltransferase 2A (MAT2A)</a>***** (help in Methionine reduced diet?)
<br>
Boswellia extracts are often administered in doses ranging from 300 mg to 1,200 mg per day<br>
<br>
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
<a href="https://www.mcsformulas.com/vitamins-supplements/boswellia-akba-liposomal/"> Boswellia MEGA AKBA</a>)<br>
AKBA also available in Inflasanum @ 90% AKDA (MCSformulas)<br>

<br>
-Note <a href="tbResList.php?qv=47&tsv=1109&wNotes=on&exSp=open">half-life</a> reports vary 2.5-90hrs?.<br>
<a href="tbResList.php?qv=47&tsv=792&wNotes=on&exSp=open">BioAv</a> (bio availability increases with high fat meal)
<br>
Pathways:<br>

<!-- ROS : MMP↓, ER Stress↑, Ca+2↑, Cyt‑c↑, Casp3↑, Casp9↑, DNAdam↑, UPR↑, cl-PARP↑-->
- induce or lower
<a href="tbResList.php?qv=47&tsv=275&wNotes=on">ROS</a> production (not consistant increase for cancer cells)<br>
- ROS↑ related:
<a href="tbResList.php?qv=47&tsv=197&wNotes=on&word=MMP↓">MMP↓</a>(ΔΨm),
<a href="tbResList.php?qv=47&tsv=103&wNotes=on">ER Stress↑</a>,
<a href="tbResList.php?qv=47&tsv=356&wNotes=on">GRP78↑</a>,
<a href="tbResList.php?qv=47&tsv=38&wNotes=on&word=Ca+2↑">Ca+2↑</a>,
<a href="tbResList.php?qv=47&tsv=77&wNotes=on">Cyt‑c↑</a>,
<a href="tbResList.php?qv=47&wNotes=on&word=Casp">Caspases↑</a>,
<a href="tbResList.php?qv=47&tsv=82&wNotes=on&word=DNAdam↑">DNA damage↑</a>,
<a href="tbResList.php?qv=47&tsv=239&wNotes=on">cl-PARP↑</a>,
<br>


- may Raise
<a href="tbResList.php?qv=47&tsv=1103&wNotes=on&word=antiOx↑">AntiOxidant</a>
defense in Normal Cells:
<a href="tbResList.php?qv=47&tsv=275&wNotes=on&word=ROS↓">ROS↓</a>,
<a href="tbResList.php?qv=47&tsv=226&wNotes=on&word=NRF2↑">NRF2↑</a>,
<a href="tbResList.php?qv=47&tsv=298&wNotes=on&word=SOD↑">SOD↑</a>,
<a href="tbResList.php?qv=47&tsv=137&wNotes=on&word=GSH↑">GSH↑</a>,
<a href="tbResList.php?qv=47&tsv=46&wNotes=on&word=Catalase↑">Catalase↑</a>,
<br>

<!-- INFLAMMATION : NF-kB↓, COX2↓, COX2↓ PRO-INFL CYTOKINES: IL-1β↓, TNF-α↓, IL-6↓, IL-8↓, -->
- lowers
<a href="tbResList.php?qv=47&tsv=953&wNotes=on&word=Inflam">Inflammation</a> :
<a href="tbResList.php?qv=47&tsv=214&wNotes=on&word=NF-kB↓">NF-kB↓</a>,
<a href="tbResList.php?qv=47&tsv=66&wNotes=on&word=COX2↓">COX2↓</a>,
<a href="tbResList.php?qv=47&tsv=235&wNotes=on&word=p38↓">p38↓</a>
(context-dependent; stress/inflammatory MAPK modulation), Pro-Inflammatory Cytokines :
<a href="tbResList.php?qv=47&tsv=978&wNotes=on&word=IL1β↓">IL-1β↓</a>,
<a href="tbResList.php?qv=47&tsv=309&wNotes=on&word=TNF-α↓">TNF-α↓</a>,
<a href="tbResList.php?qv=47&tsv=158&wNotes=on&word=IL6↓">IL-6↓</a>,
<br>



<!-- GROWTH/METASTASES : EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1, uPA↓, VEGF↓, ERK↓
inhibiting metastasis-associated proteins such as ROCK1, FAK, (RhoA), NF-κB and u-PA, MMP-1 and MMP-13.-->
- inhibit Growth/Metastases :
<a href="tbResList.php?qv=47&tsv=96&wNotes=on"EMT↓</a>,
<a href="tbResList.php?qv=47&tsv=204&wNotes=on">MMPs↓</a>,
<a href="tbResList.php?qv=47&tsv=201&wNotes=on">MMP2↓</a>,
<a href="tbResList.php?qv=47&tsv=203&wNotes=on">MMP9↓</a>,
<a href="tbResList.php?qv=47&tsv=334&wNotes=on">VEGF↓</a>,
<a href="tbResList.php?qv=47&tsv=214&wNotes=on">NF-κB↓</a>,
<a href="tbResList.php?qv=47&tsv=79&wNotes=on">CXCR4↓</a>,
<a href="tbResList.php?qv=47&tsv=105&wNotes=on">ERK↓</a>
<br>


<!-- CELL CYCLE ARREST : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓ -->
- cause Cell cycle arrest :
<a href="tbResList.php?qv=47&tsv=322&wNotes=on">TumCCA↑</a>,
<a href="tbResList.php?qv=47&tsv=73&wNotes=on">cyclin D1↓</a>,
<a href="tbResList.php?qv=47&tsv=378&wNotes=on">cyclin E↓</a>,
<a href="tbResList.php?qv=47&tsv=467&wNotes=on">CDK2↓</a>,
<a href="tbResList.php?qv=47&tsv=894&wNotes=on">CDK4↓</a>,
<a href="tbResList.php?qv=47&tsv=895&wNotes=on">CDK6↓</a>,
<br>

<!-- MIGRATION/INVASION : TumCMig↓, TumCI↓, FAK↓, ERK↓, -->
- inhibits Migration/Invasion :
<a href="tbResList.php?qv=47&tsv=326&wNotes=on">TumCMig↓</a>,
<a href="tbResList.php?qv=47&tsv=324&wNotes=on">TumCI↓</a>,
<a href="tbResList.php?qv=47&tsv=105&wNotes=on">ERK↓</a>,
<a href="tbResList.php?qv=47&tsv=1117&wNotes=on">TOP1↓</a>,
<br>



<!-- ANGIOGENESIS : VEGF↓, VEGFR2↓, HIF-1α↓, NOTCH↓, FGF↓, PDGF↓, EGFR↓ ITG(Integrins↓)-->
- inhibits
<a href="tbResList.php?qv=47&tsv=447&wNotes=on">angiogenesis↓</a> :
<a href="tbResList.php?qv=47&tsv=334&wNotes=on">VEGF↓</a>,
<a href="tbResList.php?qv=47&wNotes=on&word=NOTCH">Notch↓</a>,
<a href="tbResList.php?qv=47&tsv=361&wNotes=on">PDGF↓</a>,
<br>



<!-- OTHERS : -->
- Others: <a href="tbResList.php?qv=47&tsv=252&wNotes=on">PI3K↓</a>,
<a href="tbResList.php?qv=47&tsv=4&wNotes=on">AKT↓</a>,
<a href="tbResList.php?qv=47&wNotes=on&word=STAT">STAT↓</a>,
<a href="tbResList.php?qv=47&tsv=377&wNotes=on">Wnt↓</a>,
<a href="tbResList.php?qv=47&tsv=342&wNotes=on">β-catenin↓</a>,
<a href="tbResList.php?qv=47&tsv=9&wNotes=on">AMPK↓</a>,
<a href="tbResList.php?qv=47&tsv=105&wNotes=on">ERK↓</a>,
<a href="tbResList.php?qv=47&tsv=168&wNotes=on">JNK</a>(JNK is activated under stress)
<br>


<!-- SYNERGIES : -->
- Synergies:
<a href="tbResList.php?qv=47&tsv=1106&wNotes=on">chemo-sensitization</a>,
<a href="tbResList.php?qv=47&tsv=1171&wNotes=on">chemoProtective</a>,
<a href="tbResList.php?qv=47&tsv=1185&wNotes=on">RadioProtective</a>,
<a href="tbResList.php?qv=47&tsv=961&esv=2&wNotes=on&exSp=open">Others(review target notes)</a>,
<a href="tbResList.php?qv=47&tsv=1105&wNotes=on">Neuroprotective</a>,
<a href="tbResList.php?qv=47&tsv=557&wNotes=on">Cognitive</a>,
<a href="tbResList.php?qv=47&tsv=1179&wNotes=on">Hepatoprotective</a>,
<br>
<br>
<!-- SELECTIVE: -->
- Selectivity:
<a href="tbResList.php?qv=47&tsv=1110&wNotes=on">Cancer Cells vs Normal Cells</a><br>
<br>




<!-- Boswellia (Boswellia serrata; boswellic acids incl. AKBA) — Time-Scale Flagged Pathway Table (web-page ready) -->
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer Cells</th>
<th>Normal Cells</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>

<tr>
<td>1</td>
<td>NF-κB axis (IKK → NF-κB; NF-κB-regulated genes)</td>
<td>NF-κB ↓; downstream targets ↓ (COX-2, Cyclin D1, Bcl-2/Bcl-xL/IAPs, MMP-9, VEGF, CXCR4 etc.)</td>
<td>Anti-inflammatory tone (context)</td>
<td>R, G</td>
<td>Anti-survival / anti-inflammatory transcription</td>
<td>AKBA-class compounds suppress NF-κB signaling and reduce multiple NF-κB-regulated tumor programs in vitro and in vivo models.</td>
</tr>

<tr>
<td>2</td>
<td>5-LOX (leukotriene pathway) / eicosanoid signaling</td>
<td>5-LOX activity ↓ (context); pro-inflammatory eicosanoid signaling ↓</td>
<td>Anti-inflammatory support</td>
<td>P, R</td>
<td>Direct enzymatic / lipid-mediator suppression</td>
<td>Boswellic acids are widely discussed as 5-LOX–linked anti-inflammatory agents; cancer relevance often tracks inflammation-driven growth signals.</td>
</tr>

<tr>
<td>3</td>
<td>Apoptosis (extrinsic + intrinsic; caspases; PARP)</td>
<td>Apoptosis ↑; Caspase-8/3 ↑; cl-PARP ↑ (context)</td>
<td>↔</td>
<td>G</td>
<td>Cell death execution</td>
<td>Reported apoptosis induction includes death-receptor (e.g., DR5-associated) and caspase/PARP cleavage patterns in multiple tumor models.</td>
</tr>

<tr>
<td>4</td>
<td>Cell-cycle control (Cyclin D1 / checkpoints)</td>
<td>Cyclin D1 ↓; proliferation ↓; arrest ↑ (context)</td>
<td>↔</td>
<td>G</td>
<td>Cytostasis</td>
<td>Often presented as downstream of NF-κB/survival signaling suppression and stress adaptation.</td>
</tr>

<tr>
<td>5</td>
<td>Invasion / metastasis programs (MMP-9, ICAM-1, CXCR4)</td>
<td>Invasion markers ↓; MMP-9 ↓; ICAM-1 ↓; CXCR4 ↓ (context)</td>
<td>↔</td>
<td>G</td>
<td>Anti-invasive phenotype</td>
<td>In vivo tumor models report reductions in invasive and chemokine/migration biomarkers alongside NF-κB suppression.</td>
</tr>

<tr>
<td>6</td>
<td>Angiogenesis signaling (VEGF; VEGFR2-mediated angiogenesis)</td>
<td>VEGF ↓; angiogenic outputs ↓ (context)</td>
<td>↔</td>
<td>G</td>
<td>Anti-angiogenic support</td>
<td>AKBA has been reported to suppress angiogenesis programs including VEGF signaling, with VEGFR2-mediated angiogenesis discussed in prostate cancer contexts.</td>
</tr>

<tr>
<td>7</td>
<td>PI3K → AKT (± mTOR) survival axis</td>
<td>PI3K/AKT ↓ (reported; model-dependent)</td>
<td>↔</td>
<td>R, G</td>
<td>Growth/survival suppression</td>
<td>Commonly listed as a downstream survival pathway impacted by boswellic acids; keep as “reported” (not universal across all models).</td>
</tr>

<tr>
<td>8</td>
<td>MAPK re-wiring (ERK / JNK / p38)</td>
<td>Stress-MAPK modulation (context-dependent)</td>
<td>↔</td>
<td>P, R, G</td>
<td>Signal reprogramming</td>
<td>MAPK direction varies by tumor type/dose and whether the experimental system is inflammatory vs cytotoxic.</td>
</tr>

<tr>
<td>9</td>
<td>Chemo-/radio-sensitization (combination relevance)</td>
<td>Sensitization ↑ (context)</td>
<td>—</td>
<td>G</td>
<td>Combination leverage</td>
<td>Combination studies report enhanced tumor control when AKBA-class compounds are paired with other therapies (context and regimen dependent).</td>
</tr>

<tr>
<td>10</td>
<td>Bioavailability constraint (oral exposure; formulation dependence)</td>
<td>Systemic exposure often limited without enhanced delivery</td>
<td>—</td>
<td>—</td>
<td>Translation constraint</td>
<td>Poor pharmacokinetics are a common limitation; multiple strategies (e.g., micellar delivery, bioenhancers) are studied to improve absorption.</td>
</tr>
</table>

<p><b>Time-Scale Flag (TSF):</b> P / R / G</p>
<ul>
<li><b>P</b>: 0–30 min (primary/physical–chemical effects; rapid enzymatic/kinase shifts)</li>
<li><b>R</b>: 30 min–3 hr (acute redox + stress-response signaling)</li>
<li><b>G</b>: &gt;3 hr (gene-regulatory adaptation and phenotype-level outcomes)</li>
</ul>