condition found tbRes List
CAP, Capsaicin: Click to Expand ⟱
Features:
Capsaicin is a chemical compound that gives chili peppers their spicy flavor and heat.

Biological activity, capsaicin has been reported to exhibit a range of effects, including:
Pain relief: 10-50 μM
Anti-inflammatory activity: 20-50 μM
Antioxidant activity: 10-100 μM
Anti-cancer activity: 50-100 μM
Cardiovascular health: 20-50 μM

Approximate μM concentrations of capsaicin, the active compound in chili peppers, that can be achieved with different amounts of chili peppers:
1 teaspoon of dried chili pepper flakes (5g):~10-50 μM of capsaicin
1 tablespoon of dried chili pepper flakes (15g): ~30-150 μM of capsaicin
1 cup of fresh chili peppers (100g): ~100-500 μM of capsaicin
1 teaspoon of chili pepper extract (5g): ~100-500 μM of capsaicin
1 tablespoon of chili pepper extract (15g): ~300-1500 μM of capsaicin

Approximate μM concentrations of capsaicin in various foods that contain capsaicin:
Jalapeño peppers: 1 pepper (20g): ~20-100 μM of capsaicin 2–8 mg/100g of fresh Jalapeño
Serrano peppers: 1 pepper (10g): ~10-50 μM of capsaicin 5–15 mg/100g
Cayenne peppers: 1 pepper (10g): ~50-200 μM of capsaicin
Habanero peppers: 1 pepper (20g): ~100-500 μM of capsaicin 15–30 mg/100g
Ghost peppers: 1 pepper (20g): ~200-1000 μM of capsaicin
Hot sauce: 1 teaspoon (5g): ~10-50 μM of capsaicin
Chili flakes: 1 teaspoon (5g): ~10-50 μM of capsaicin
Spicy sauces and marinades: 1 tablespoon (15g): ~10-50 μM of capsaicin

Cayenne Pepper Powder – Approximate capsaicin content: roughly 5–20 mg/g (15-30g human for 100uM?)

-IC50 in Cancer Cell Lines: Approximately 50–300 µM (consume 150mg of capsaican not possible?)
-IC50 in Normal Cell Lines: Generally higher—often 2–3 times greater

Pathways:
-disrupting mitochondrial membrane potential, leading to cytochrome c release and subsequent activation of caspases
-Activation of TRPV1: resulting in increased intracellular calcium levels
-capsaicin can lead to increased production of ROS within cancer cells
-Inhibition of NF-κB
-Inhibit PI3K/AKT/mTOR signaling
-STAT3 Inhibition
-Cell Cycle Arrest
-reduce the expression of vascular endothelial growth factor (VEGF)
-COX-2
selectivity, selectivity: Click to Expand ⟱
Source:
Type:
The selectivity of cancer products (such as chemotherapeutic agents, targeted therapies, immunotherapies, and novel cancer drugs) refers to their ability to affect cancer cells preferentially over normal, healthy cells. High selectivity is important because it can lead to better patient outcomes by reducing side effects and minimizing damage to normal tissues.

Achieving high selectivity in cancer treatment is crucial for improving patient outcomes. It relies on pinpointing molecular differences between cancerous and normal cells, designing drugs or delivery systems that exploit these differences, and overcoming intrinsic challenges like tumor heterogeneity and resistance

Factors that affect selectivity:
1. Ability of Cancer cells to preferentially absorb a product/drug
-EPR-enhanced permeability and retention of cancer cells
-nanoparticle formations/carriers may target cancer cells over normal cells
-Liposomal formations. Also negatively/positively charged affects absorbtion

2. Product/drug effect may be different for normal vs cancer cells
- hypoxia
- transition metal content levels (iron/copper) change probability of fenton reaction.
- pH levels
- antiOxidant levels and defense levels

3. Bio-availability
Scientific Papers found: Click to Expand⟱
2020- CAP,    Capsaicinoids and Their Effects on Cancer: The “Double-Edged Sword” Postulate from the Molecular Scale
- Review, Var, NA
AntiTum↑, highlighting its antitumor properties mediated by cytotoxicity and immunological adjuvancy against at least 74 varieties of cancer,
selectivity↑, while non-cancer cells tend to have greater tolerance
TRPV1↑, activation or phosphorylation of TRPV1
MMP↓, leads to cell membrane depolarization through the influx of Na2+ and Ca2+,
Ca+2↑,
ER Stress↑, endoplasmic reticulum stress [73], and the inhibition of angiogenesis
angioG↓,
Casp3?, increase in caspase-3 activation, PARP-1 cleavage
cl‑PARP↑,
selectivity↑, oxidative stress threshold reached by these could be potentially higher than that caused in normal cells (tNOX−) when exposed to CAP, possibly also contributing to the selectivity of its effects
ROS↑, increase in the production of reactive oxygen species (ROS),
*ROS∅, Remarkably, in this same work, cells derived from the normal epithelium of human pancreatic ducts (HPDE6-E6E7) showed high tolerance to the same treatment by keeping their ROS levels stable
selectivity↑, In this sense, non-transformed human astrocytes from a primary culture showed greater tolerance to CAP, as they did not experience any of the mentioned effects when exposed to the same treatment

2019- CAP,    Capsaicin: A Two-Decade Systematic Review of Global Research Output and Recent Advances Against Human Cancer
- Review, Var, NA
chemoP↑, Capsaicin has shown significant prospects as an effective chemopreventive agent
Ca+2↑, Capsaicin was shown to cause upstream activation of Ca2+
antiOx↑, Another plausible mechanism implicated in the chemopreventive action of capsaicin is its anti-oxidative effects.
*ROS↓, capsaicin inhibits ROS release and the subsequent mitochondrial membrane potential collapse, cytochrome c expression, chromosome condensation, and caspase-3 activation induced by oxidized low-density lipoprotein in normal human HUVEC cells
*MMP∅,
*Cyt‑c∅,
*Casp3∅,
*eff↑, dietary curcumin and capsaicin concurrent administration in high-fat diet-fed rats were shown to mitigate the testicular and hepatic antioxidant status by increasing GSH levels, glutathione transferase activity, and Cu-ZnSOD expression
*Inflam↓, Anti-inflammation is another mechanism implicated in the chemopreventive action of capsaicin.
*NF-kB↓, inhibition of NF-kB by capsaicin
*COX2↓, compound elicits COX-2 enzyme activity inhibition and downregulation of iNOS
iNOS↓,
TRPV1↑, major pro-apoptotic mechanisms of capsaicin is via the vanilloid receptors, primarily TRPV1
i-Ca+2?, causing a concomitant influx of Ca2+: severe condition of mitochondria calcium overload. at high concentration (> 10 µM), capsaicin induces a slow but persistent increase in intracellular Ca2+
MMP↓, depolarization of mitochondria membrane potential
Cyt‑c↑, release of cytochrome C
Bax:Bcl2↑, activation of Bax and p53 through C-jun N-terminal kinase (JNK) activation
P53↑,
JNK↑,
PI3K↓, blocking the Pi3/Akt/mTOR signalling pathway, capsaicin increases levels of autophagic markers (LC3-II and Atg5)
Akt↓,
mTOR↓,
LC3II↑,
ATG5↑,
p62↑, enhances p62 and Fap-1 degradation and increases caspase-3 activity to induce apoptosis in human nasopharyngeal carcinoma cells
Fap1↓,
Casp3↑,
Apoptosis↑,
ROS↑, generation of ROS in human hepatoma (HepG2 cells)
MMP9↓, inhibition of MMP9 by capsaicin occurs via the suppression of AMPK-NF-κB, EGFR-mediated FAK/Akt, PKC/Raf/ERK, p38 MAPK, and AP-1 signaling pathway
eff↑, capsaicin 8% patch could promote the regeneration and restoration of skin nerve fibres in chemotherapy-induced peripheral neuropathy in addition to pain relief
eff↓, capsaicin has shown several unpleasant side effects, including stomach cramps, skin and gastric irritation, and burning sensation
eff↑, liposomes and micro-emulsion-based drugs have been known to significantly improve oral bioavailability and reduce the irritation of drugs
selectivity↑, In addition, these delivery systems can be surfaced-modified to perform site-directed/cell-specific drug delivery, thereby ensuring increased cell death of cancer cells while sparing non-selective normal cells
eff↑, Furthermore, owing to its antioxidant potential, capsaicin has been applied as a bioreduction and capping agent to synthesize biocompatible silver nanoparticles
ChemoSen↑, capsaicin has been combined with other anticancer therapies for more pronounced anticancer effects

2018- CAP,  MF,    Capsaicin: Effects on the Pathogenesis of Hepatocellular Carcinoma
- Review, HCC, NA
TRPV1↑, Capsaicin is an agonist for transient receptor potential cation channel subfamily V member 1 (TRPV1)
eff↑, It is noteworthy that capsaicin binding to the TRPV1 receptor may be increased using a static magnetic field (SMF), thus enhancing the anti-cancer effect of capsaicin on HepG2 (human hepatoblastoma cell line) cells through caspase-3 apoptosis
Akt↓, capsaicin can regulate autophagy by inhibiting the Akt/mTOR
mTOR↓,
p‑STAT3↑, Capsaicin can upregulate the activity of the signal transducer and activator of transcription 3 (p-STAT3)
MMP2↑, increase of the expression of MMP-2
ER Stress↑, capsaicin may induce apoptosis through endoplasmic reticulum (ER) stress
Ca+2↑, and the subsequent ER release of Ca2+
ROS↑, Capsaicin-induced ROS generation
selectivity↑, On the other hand, an excess of capsaicin is cytotoxic on HepG2 cells, and normal hepatocytes to a smaller extent, by collapse of the mitochondrial membrane potential with ROS formation
MMP↓,
eff↑, combination of capsaicin and sorafenib demonstrated significant anticarcinogenic properties on LM3 HCC cells, restricting tumor cell growth

2015- CAP,  CUR,  urea,    Anti-cancer Activity of Sustained Release Capsaicin Formulations
- Review, Var, NA
AntiCan↑, Several convergent studies show that capsaicin displays robust cancer activity, suppressing the growth, angiogenesis and metastasis of several human cancers.
TumCG↓,
angioG↓,
TumMeta↓,
BioAv↓, clinical applications of capsaicin as a viable anti-cancer drug have remained problematic due to its poor bioavailability and aqueous solubility properties
BioAv↓, capsaicin is associated with adverse side effects like gastrointestinal cramps, stomach pain, nausea and diarrhea and vomiting
BioAv↑, All these hurdles may be circumvented by encapsulation of capsaicin in sustained release drug delivery systems.
selectivity↑, Most importantly, these long-acting capsaicin formulations selectively kill cancer cells and have minimal growth-suppressive activity on normal cells.
EPR↑, The EPR effect is a mechanism by which high–molecular drug delivery systems (typically prodrugs, liposomes, nanoparticles, and macromolecular drugs) tend to accumulate in tumor tissue much more than they do in normal tissues
eff↓, The efficiency of such extravasation is maximum when the size of the liposomes less than 200 nm The CAP-CUR-GLY-GAL-LIPO were spherical in shape with a narrow range of size distribution ranging from 135–155nm
ChemoSen↑, The chemosensitization and anti-tumor activity of capsaicin involves multiple molecular pathways
Dose∅, oral, Intravenous (IV), and Intraperitoneal (IP) options
Half-Life∅, oral metabolized in 105mins, T1/2in blood=25mins.
eff↑, presence of urea (as a carrier) increased the aqueous solubility of capsaicin by 3.6-fold compared to pure capsaicin

2014- CAP,    Role of Mitochondrial Electron Transport Chain Complexes in Capsaicin Mediated Oxidative Stress Leading to Apoptosis in Pancreatic Cancer Cells
- in-vitro, PC, Bxpc-3 - in-vitro, Nor, HPDE-6 - in-vivo, PC, AsPC-1
ROS↑, ROS was about 4–6 fold more as compared to control and as early as 1 h after capsaicin treatment in BxPC-3 and AsPC-1 cells
*ROS∅, but not in normal HPDE-6 cells
selectivity↑, only small ~1.2fold ROS increase in normal cell
compI↓, capsaicin inhibits about 2.5–9% and 5–20% of complex-I activity
compIII↓, and 8–75% of complex-III activity in BxPC-3 and AsPC-1 cells respectively
eff↑, which was attenuable by SOD, catalase and EUK-134.
selectivity↑, capsaicin treatment failed to inhibit complex-I or complex-III activities in normal HPDE-6 cells
ATP↓, ATP levels were drastically suppressed by capsaicin treatment in both BxPC-3 and AsPC-1 cells
Cyt‑c↑, release of cytochrome c and cleavage of both caspase-9 and caspase-3 due to disruption of mitochondrial membrane potential
Casp9↑,
Casp3↑,
MMP↓,
SOD↓, mice orally fed with 2.5 mg/kg capsaicin show decreased SOD activity and an increase in GSSG/GSH levels as compared to controls
GSH/GSSG↓, mice orally fed with 2.5 mg/kg capsaicin
Apoptosis↑, Capsaicin triggers apoptosis in pancreatic cancer cells but not in normal HPDE-6 cells
*toxicity∅, Capsaicin triggers apoptosis in pancreatic cancer cells but not in normal HPDE-6 cells
GSH↓, Taken together, our results suggest that depletion of GSH level and inhibition of SOD, catalase and GPx by capsaicin disturbs the cellular redox homeostasis resulting in increased oxidative stress.
Catalase↓,
GPx↓,
Dose↝, 13.2 mg dose of capsaicin for a 60 kg person


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Results for Effect on Cancer/Diseased Cells:
Akt↓,2,   angioG↓,2,   AntiCan↑,1,   antiOx↑,1,   AntiTum↑,1,   Apoptosis↑,2,   ATG5↑,1,   ATP↓,1,   Bax:Bcl2↑,1,   BioAv↓,2,   BioAv↑,1,   Ca+2↑,3,   i-Ca+2?,1,   Casp3?,1,   Casp3↑,2,   Casp9↑,1,   Catalase↓,1,   chemoP↑,1,   ChemoSen↑,2,   compI↓,1,   compIII↓,1,   Cyt‑c↑,2,   Dose↝,1,   Dose∅,1,   eff↓,2,   eff↑,7,   EPR↑,1,   ER Stress↑,2,   Fap1↓,1,   GPx↓,1,   GSH↓,1,   GSH/GSSG↓,1,   Half-Life∅,1,   iNOS↓,1,   JNK↑,1,   LC3II↑,1,   MMP↓,4,   MMP2↑,1,   MMP9↓,1,   mTOR↓,2,   P53↑,1,   p62↑,1,   cl‑PARP↑,1,   PI3K↓,1,   ROS↑,4,   selectivity↑,8,   SOD↓,1,   p‑STAT3↑,1,   TRPV1↑,3,   TumCG↓,1,   TumMeta↓,1,  
Total Targets: 51

Results for Effect on Normal Cells:
Casp3∅,1,   COX2↓,1,   Cyt‑c∅,1,   eff↑,1,   Inflam↓,1,   MMP∅,1,   NF-kB↓,1,   ROS↓,1,   ROS∅,2,   toxicity∅,1,  
Total Targets: 10

Scientific Paper Hit Count for: selectivity, selectivity
5 Capsaicin
1 Magnetic Fields
1 Curcumin
1 urea
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:55  Target#:1110  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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