condition found tbRes List
RosA, Rosmarinic acid: Click to Expand ⟱
Features: polyphenol
Polyphenol of many herbs - rosemary, perilla, sage mint and basil. Rosmarinic acid (RA) is predominantly found in a variety of medicinal and culinary herbs, especially those belonging to the Lamiaceae family, including rosemary (Rosmarinus officinalis), basil (Ocimum basilicum), sage (Salvia officinalis), thyme (Thymus vulgaris), and mints (Mentha spp.). In addition to the Lamiaceae family, RA is also present in plants from other families, such as Boraginaceae and Apiaceae.
-Rosmarinic acid is one of the hydroxycinnamic acids, and was initially isolated and purified from the extract of rosemary, a member of mint family (Lamiaceae)
-Its chemical structure allows it to act as a free radical scavenger by donating hydrogen atoms to stabilize ROS and free radicals.
RA’s dual nature as both a phenolic acid and a flavonoid-related compound enables it to chelate metal ions and prevent the formation of free radicals, thus interrupting oxidative chain reactions. It can modulate the activity of enzymes involved in OS, such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), underscoring its potential role in preventing oxidative damage at the cellular level.
-divided as rosemary extract, carnosic acid, rosmarinic acid?

Summary:
-Capacity to chelate transition metal ions, particularly ironChelator (Fe2+) and copper (Cu2+)
-RA plus Cu(II)-induced oxidative DNA damage, which causes ROS
-rosmarinic acid (RA) as a potential inhibitor of MARK4↓ (inhibiting to tumor growth, invasion, and metastasis) activity (IC50 = 6.204 µM)

-Note half-life 1.5–2 hours.
BioAv water-soluble, rapid absorbtion
Pathways:
- varying results of ROS up or down in cancer cells. Plus a report of lowering ROS and no effect on Tumor cell viability.
However always seems to lower ROS↓ in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓,
- No indication of Lowering AntiOxidant defense in Cancer Cells:
- Raises AntiOxidant defense in Normal Cells:(and perhaps even in cancer cells) ROS↓, NRF2↑***, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, VEGF↓, ROCK1↓, RhoA↓, NF-κB↓, ERK↓, MARK4↓
- reactivate genes thereby inhibiting cancer cell growth(weak) : HDAC2↓, DNMTs↓weak, P53↑, HSP↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓??, LDHA↓, PFKs↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, EGFR↓,
- inhibits Cancer Stem Cells (few references) : CSC↓, Hh↓, GLi1↓,
- Others: PI3K↓, AKT↓, STAT↓, AMPK, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


neuroP, neuroprotective: Click to Expand ⟱
Source:
Type:
Neuroprotective refers to the ability of a substance, intervention, or strategy to preserve the structure and function of nerve cells (neurons) against injury or degeneration.
-While cancer and neurodegenerative processes might seem distinct, there is significant overlap in terms of treatment-related neurotoxicity, shared molecular mechanisms, and the potential for therapies that provide neuroprotection during cancer treatment.
Scientific Papers found: Click to Expand⟱
3022- RosA,    Rosmarinic acid against cognitive impairment via RACK1/HIF-1α regulated microglial polarization in sepsis-surviving mice
- in-vitro, Sepsis, NA
*cognitive↑, Rosmarinic acid alleviates cognitive impairment and glycolytic metabolism abnormality in sepsis mice model.
*neuroP↑, Rosmarinic acid attenuates neuronal injury and microglial activation.
*GlucoseCon↑, promoted whole-brain glucose uptake in mice.
*Hif1a↓, (rescued the decrease of RACK1 and increase of HIF-1α)

3028- RosA,    Network pharmacology mechanism of Rosmarinus officinalis L.(Rosemary) to improve cell viability and reduces apoptosis in treating Alzheimer’s disease
- in-vitro, AD, HT22 - in-vivo, NA, NA
*Aβ↓, It was found that rosemary could reversed Aβ25–35 induced damage to mouse hippocampal neuron HT22 cells,
*Apoptosis↓, significantly improved the viability of damaged cells, and reduced apoptosis
*antiOx↓, main antioxidant compound in rosemary, carnosic acid, also has neuroprotective effects.
*neuroP↑,
*eff↑, main active carnosic acid, carnosol, rosmarinol, rosmadial, genkwanin, cirsimaritin, rosmarinic acid and caffeic acid in Rosmarinus officinalis L,
*IGF-1↑, rosemary could elevated expression of IGF1, MMP9 and decreased mRNA levels of SRC, MAPK14, compared with the control group.
*MMP9↑,
*Src↓,
*MAPK↓,
*MMP↑, Rosemary reduced Aβ-induced HT22 cell damage in AD models to enhance the mitochondrial membrane potential levels

3039- RosA,    Rosmarinic acid liposomes suppress ferroptosis in ischemic brain via inhibition of TfR1 in BMECs
- in-vivo, Nor, NA - in-vivo, Stroke, NA
*Ferroptosis↓, RosA-LIP inhibited ferroptosis by ameliorating mitochondrial abnormalities, increasing GPX4 levels, and decreasing ACSL4/LPCAT3/Lox-dependent lipid peroxidation.
*GPx4↑,
*ACSL4↓,
*BBB↑, RosA-LIP effectively improved blood‒brain barrier (BBB) permeability, increased tight junctions (TJs) protein expression
*IronCh↑, reduced iron levels in ischemic tissue and brain microvascular endothelial cells (BMECs) by modulating FPN1 and TfR1 levels.
*TfR1/CD71↓, Furthermore, RosA-LIP suppressed TfR1 to attenuate ACSL4/LPCAT3/Lox-mediated ferroptosis in TfR1EC cKO mice subjected to dMCAO.
*neuroP↑, proposed neuroprotection of RosA-LIP during ischemic stroke.

3003- RosA,    Comprehensive Insights into Biological Roles of Rosmarinic Acid: Implications in Diabetes, Cancer and Neurodegenerative Diseases
- Review, Var, NA - Review, AD, NA - Review, Park, NA
*Inflam↓, anti-inflammatory and antioxidant properties and its roles in various life-threatening conditions, such as cancer, neurodegeneration, diabetes,
*antiOx↑,
*neuroP↑,
*IL6↓, diabetic rat model treated with RA, there is an anti-inflammatory activity reported. This activity is achieved through the inhibition of the expression of various proinflammatory factors, including in IL-6, (IL-1β), tumour
*IL1β↓,
*NF-kB↓, inhibiting NF-κB activity and reducing the production of prostaglandin E2 (PGE2), nitric oxide (NO), and cyclooxygenase-2 (COX-2) in RAW 264.7 cells.
*PGE2↓,
*COX2↓,
*MMP↑, RA inhibits cytotoxicity in tumour patients by maintaining the mitochondrial membrane potential
*memory↑, amyloid β(25–35)-induced AD in rats was treated with RA, which mitigated the impairment of learning and memory disturbance by reducing oxidative stress
*ROS↓,
*Aβ↓, daily consumption of RA diminished the effect of neurotoxicity of Aβ25–35 in mice
*HMGB1↓, SH-SY5Y in vitro and ischaemic diabetic stroke in vivo, and the studies revealed that a 50 mg/kg dose of RA decreased HMGB1 expression
TumCG↓, Rosemary and its extracts have been shown to exhibit potential in inhibiting the growth of cancer cells and the development of tumours in various cancer types, including colon, breast, liver, and stomach cancer
MARK4↓, Another study reported the inhibition of Microtubule affinity regulating kinase 4 (MARK4) by RA
Zeb1↓, Fig 4 BC:
MDM2↓,
BNIP3↑,
ASC↑, Skin Cancer
NLRP3↓,
PI3K↓,
Akt↓,
Casp1↓,
E-cadherin↑, Colon Cancer
STAT3↓,
TLR4↓,
MMP↓,
ICAM-1↓,
AMPK↓,
IL6↑, PC and GC
MMP2↓,
Warburg↓,
Bcl-xL↓, CRC: Apoptosis induction caspases ↑, Bcl-XL ↓, BCL-2 ↓, Induces cell cycle arrest, Inhibition of EMT and invasion, Reduced metastasis
Bcl-2↓,
TumCCA↑,
EMT↓,
TumMeta↓,
mTOR↓, Inhibits mTOR/S6K1 pathway to induce apoptosis in cervical cancer
HSP27↓, Glioma ↓ expression of HSP27 ↑ caspase-3
Casp3↑,
GlucoseCon↓, GC: Inhibited the signs of the Warburg effect, such as high glucose consumption/anaerobic glycolysis, lactate production/cell acidosis, by inhibiting the IL-6/STAT3 pathway
lactateProd↓,
VEGF↓, ↓ angiogenic factors (VEGF) and phosphorylation of p65
p‑p65↓,
GIT1↓, PC: Increased degradation of Gli1
Foxm1↓, inhibiting FOXM1
cycD1↓, RA treatment in CRC cells inhibited proliferation-induced cell cycle arrest of the G0/G1 phase by reducing the cyclin D1 and CDK4 levels,
CDK4↓,
MMP9↓, CRC cells, and it led to a decrease in the expressions of matrix metalloproteinase (MMP)-2 and MMP-9.
HDAC2↓, PCa cells through the inhibition of HDAC2

1745- RosA,    Rosmarinic acid and its derivatives: Current insights on anticancer potential and other biomedical applications
- Review, Var, NA - Review, AD, NA
ChemoSideEff↓, updated review is to highlight the chemopreventive and chemotherapeutic effects of RA and its derivatives
ChemoSen↑,
antiOx↑, RA also showed antioxidant effects and suppressed the activity and expression of matrix metalloproteinase (MMP)− 2,9
MMP2↓,
MMP9↓,
p‑AMPK↑, show that RA prevents metastasis through AMPK phosphorylation and suppresses CRC cell growth
DNMTs↓, RA allegedly suppressed DNA methyltransferase activity in the human breast cancer MCF7 cell line
tumCV↓, A549 lung cancer cells were 50% suppressed by RA, which also prevented COX-2 activity in these cells.
COX2↓,
E-cadherin↑, upregulating E-cadherin expression while downregulating Vimentin and N-cadherin expression, indicating that RA could inhibit hepatocellular carcinoma cells' ability to invade by MMPs and EMT
Vim↓,
N-cadherin↓,
EMT↓,
Casp3↑, The activation of caspase-3 and caspase-9 by RA also prevented the migration and invasion of liver cancer cells
Casp9↓,
ROS↓, In addition to reducing ROS, RA also enhanced GSH synthesis, lowered the expression of MMP-2 and MMP-9
GSH↑,
ERK↓, By inhibiting ERK and Akt activation, RA may stop the progression of colon cancer
Akt↓,
ROS↓, In U937 cells, it has been demonstrated that treatment with RA in concentrations 60 µM suppresses ROS and NF-kB by blocking IκB-α from being phosphorylated and degraded and the nuclear translocation of p50 and p65
NF-kB↓,
p‑IκB↓,
p50↓,
p65↓,
neuroP↑, RA can prevent the pathophysiology of Alzheimer's disease by reducing Aβ aggregation
Dose↝, 60 µM suppresses ROS and NF-kB by blocking IκB-α from being phosphorylated and degraded and the nuclear translocation of p50 and p65

3001- RosA,    Therapeutic Potential of Rosmarinic Acid: A Comprehensive Review
- Review, Var, NA
TumCP↓, including in tumor cell proliferation, apoptosis, metastasis, and inflammation
Apoptosis↑,
TumMeta↓,
Inflam↓,
*antiOx↑, RA is therefore considered to be the strongest antioxidant of all hydroxycinnamic acid derivatives
*AntiAge↑, , it also exerts powerful antimicrobial, anti-inflammatory, antioxidant and even antidepressant, anti-aging effects
*ROS↓, RA and its metabolites can directly neutralize reactive oxygen species (ROS) [10] and thereby reduce the formation of oxidative damage products.
BioAv↑, RA is water-soluble, and according to literature data, the efficacy of secretion of this compound in infusions is about 90%
Dose↝, Accordingly, it is possible to consume approximately 110 mg RA daily, i.e., approximately 1.6 mg/kg for adult men weighing 70 kg.
NRF2↑, liver cancer cell line, HepG2, transfected with plasmid containing ARE-luciferin gene, RA predominantly enhances ARE-luciferin activity and promotes nuclear factor E2-related factor-2 (Nrf2) translocation from cytoplasm to the nucleus
P-gp↑, and also increases MRP2 and P-gp efflux activity along with intercellular ATP level
ATP↑,
MMPs↓, RA concurrently induced necrosis and apoptosis and stimulated MMP dysfunction activated PARP-cleavage and caspase-independent apoptosis.
cl‑PARP↓,
Hif1a↓, inhibits transcription factor hypoxia-inducible factor-1α (HIF-1α) expression
GlucoseCon↓, it also suppressed glucose consumption and lactate production in colorectal cells
lactateProd↓,
Warburg↓, may suppress the Warburg effects through an inflammatory pathway involving activator of transcription-3 (STAT3) and signal transducer of interleukin (IL)-6
TNF-α↓, RA supplementation also reduced tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2) and IL-6 levels, and modulated p65 expression [
COX2↓,
IL6↓,
HDAC2↓, RA induced the cell cycle arrest and apoptosis in prostate cancer cell lines (PCa, PC-3, and DU145) [31]. These effects were mediated through modulation of histone deacetylases expression (HDACs), specifically HDAC2;
GSH↑, RA can also inhibit adhesion, invasion, and migration of Ls 174-T human colon carcinoma cells through enhancing GSH levels and decreasing ROS levels
ROS↓,
ChemoSen↑, RA also enhances chemosensitivity of human resistant gastric carcinoma SGC7901 cells
*BG↓, RA significantly increased insulin index sensitivity and reduced blood glucose, advanced glycation end-products, HbA1c, IL-1β, TNFα, IL-6, p-JNK, P38 mitogen-activated protein kinase (MAPK), and NF-κB levels
*IL1β↓,
*TNF-α↓,
*IL6↓,
*p‑JNK↓,
*p38↓,
*Catalase↑, The reduced activities of CAT, SOD, glutathione S-transferases (GST), and glutathione peroxidase (GPx) and the reduced levels of vitamins C and E, ceruloplasmin, and GSH in plasma of diabetic rats were also significantly recovered by RA application
*SOD↑,
*GSTs↑,
*VitC↑,
*VitE↑,
*GSH↑,
*GutMicro↑, protective effects of RA (30 mg/kg) against hypoglycemia, hyperlipidemia, oxidative stress, and an imbalanced gut microbiota architecture was studied in diabetic rats.
*cardioP↑, Cardioprotective Activity: RA also reduced fasting serum levels of vascular cell adhesion molecule 1 (VCAM-1), inter-cellular adhesion molecule 1 (ICAM-1), plasminogen-activator-inhibitor-1 (PAI-1), and increased GPX and SOD levels
*ROS↓, Finally, in H9c2 cardiac muscle cells, RA inhibited apoptosis by decreasing intracellular ROS generation and recovering mitochondria membrane potential
*MMP↓,
*lipid-P↓, At once, RA suppresses lipid peroxidation (LPO) and ROS generation, whereas in HSC-T6 cells it increases cellular GSH.
*NRF2↑, Additionally, it significantly increases Nrf2 translocation
*hepatoP↑, Hepatoprotective Activity
*neuroP↑, Nephroprotective Activity
*P450↑, RA also reduced CP-produced oxidative stress and amplified cytochrome P450 2E1 (CYP2E1), HO-1, and renal-4-hydroxynonenal expression.
*HO-1↑,
*AntiAge↑, Anti-Aging Activity
*motorD↓, A significantly delays motor neuron dysfunction in paw grip endurance tests,

3006- RosA,    Rosmarinic acid attenuates glioblastoma cells and spheroids’ growth and EMT/stem-like state by PTEN/PI3K/AKT downregulation and ERK-induced apoptosis
- in-vitro, GBM, U87MG - in-vitro, GBM, LN229
TumCG↓, Rosmarinic acid (RA) reduced the glioma growth and motility in 2D- and 3D-cultures
EMT↓, RA suppressed epithelial-mesenchymal transition and stem-cell property in spheroids.
SIRT1↓, RA downregulated SIRT1/FOXO1/NF-κB axis independently of p53 or PTEN function.
FOXO1↓,
NF-kB↓,
angioG↓, RA dose-dependently reduced angiogenesis and intracellular ROS levels, suppressed glioma growth,
ROS↓,
PTEN↓, RA also inhibited the PTEN/PI3K/AKT pathway in U-87MG cells.
PI3K↓,
Akt↓,
*Inflam↓, anti-inflammatory, antimicrobial, cardioprotective, hepatoprotective, neuroprotective, antidiabetic, and especially anticancer effects (
*cardioP↑,
*hepatoP↑,
*neuroP↑,
Warburg↓, suppresses Warburg effect

3007- RosA,    Hepatoprotective effects of rosmarinic acid: Insight into its mechanisms of action
- Review, NA, NA
*ROS↓, antioxidant properties as a ROS scavenger and lipid peroxidation inhibitor, anti-inflammatory, neuroprotective and antiangiogenic among others.
*lipid-P↓,
*Inflam↓,
*neuroP↑,
*angioG↓,
*eff↑, The hepatoprotective effects of RA alone and in combination with caffeic acid (CA) was reported in t-BHP-induced oxidative liver damage
*AST↓, significant reduction of indicators of hepatic toxicity, such as AST, ALT, GSSG, lipid peroxidation.
*ALAT↓,
*GSSG↓,
*eNOS↓, It also reduced the liver content of eNOS/iNOS and NO, attenuated NF-κB activation
*iNOS↓,
*NO↓,
*NF-kB↓,
*MMP2↓, It inhibited MMP-2 activity and suppressed ROS generation and lipid peroxidation.
*MDA↓, It also decreased malondialdehyde (MDA) and TNF-α levels while increasing GSH levels as well as SOD and GSH-Px activities in the livers and kidneys.
*TNF-α↓,
*GSH↑,
*SOD↑,
*IL6↓, RA decreased the hepatic level of IL-6, TNF-Alpha, and PGE2, as well as the activity of COX-2 It also decreased hepatic RAGE and sorbitol levels, and GLO-1 activity
*PGE2↓,
*COX2↓,
*mTOR↑, In the study, it was observed that RA stimulated hepatocyte proliferation. Specifically activated the mTOR signaling pathway during liver regeneration and rescued PH-impaired liver functions

3014- RosA,    Rosmarinic Acid Supplementation Acts as an Effective Antioxidant for Restoring the Antioxidation/Oxidation Balance in Wistar Rats with Cadmium-Induced Toxicity
- in-vivo, Nor, NA
*antiOx↑, Rats in Group 4 (cadmium-exposed and Rosmarinic acid-accessed) exhibited increased levels of total proteins, a significant increase in the levels of antioxidant markers including total thiols, glutathione, total antioxidant capacity (TAC),
*Thiols↑,
*GSH↑,
*TAC↑, decreased levels of total thiols, GSH, catalase, and TAC
*SOD↑, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase, and a significant decrease in the levels of blood cadmium, ALP, ALT, AST, creatinine, blood urea nitrogen (BUN), urea, bilirubin, and oxidation markers (H2O2, and MDA
*GPx↑,
*Catalase↑,
*ALP↓,
*ALAT↓,
*AST↓,
*creat↓,
*BUN↓,
*H2O2↓,
*MDA↓,
*ROS↓, significantly help attenuate the oxidative stress induced by cadmium
cardioP↑, benefits of RA are attributed to its anti-cancer, anti-depressive, antiallergic, anti-inflammatory, anti-angiogenic, cardioprotective, hepatoprotective, nephroprotective, neuroprotective, antimicrobial, hypoglycemic, and hypolipidemic bioactivities
hepatoP↑,
neuroP↑,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Results for Effect on Cancer/Diseased Cells:
Akt↓,3,   AMPK↓,1,   p‑AMPK↑,1,   angioG↓,1,   antiOx↑,1,   Apoptosis↑,1,   ASC↑,1,   ATP↑,1,   Bcl-2↓,1,   Bcl-xL↓,1,   BioAv↑,1,   BNIP3↑,1,   cardioP↑,1,   Casp1↓,1,   Casp3↑,2,   Casp9↓,1,   CDK4↓,1,   ChemoSen↑,2,   ChemoSideEff↓,1,   COX2↓,2,   cycD1↓,1,   DNMTs↓,1,   Dose↝,2,   E-cadherin↑,2,   EMT↓,3,   ERK↓,1,   Foxm1↓,1,   FOXO1↓,1,   GIT1↓,1,   GlucoseCon↓,2,   GSH↑,2,   HDAC2↓,2,   hepatoP↑,1,   Hif1a↓,1,   HSP27↓,1,   ICAM-1↓,1,   IL6↓,1,   IL6↑,1,   Inflam↓,1,   p‑IκB↓,1,   lactateProd↓,2,   MARK4↓,1,   MDM2↓,1,   MMP↓,1,   MMP2↓,2,   MMP9↓,2,   MMPs↓,1,   mTOR↓,1,   N-cadherin↓,1,   neuroP↑,2,   NF-kB↓,2,   NLRP3↓,1,   NRF2↑,1,   P-gp↑,1,   p50↓,1,   p65↓,1,   p‑p65↓,1,   cl‑PARP↓,1,   PI3K↓,2,   PTEN↓,1,   ROS↓,4,   SIRT1↓,1,   STAT3↓,1,   TLR4↓,1,   TNF-α↓,1,   TumCCA↑,1,   TumCG↓,2,   TumCP↓,1,   tumCV↓,1,   TumMeta↓,2,   VEGF↓,1,   Vim↓,1,   Warburg↓,3,   Zeb1↓,1,  
Total Targets: 74

Results for Effect on Normal Cells:
ACSL4↓,1,   ALAT↓,2,   ALP↓,1,   angioG↓,1,   AntiAge↑,2,   antiOx↓,1,   antiOx↑,3,   Apoptosis↓,1,   AST↓,2,   Aβ↓,2,   BBB↑,1,   BG↓,1,   BUN↓,1,   cardioP↑,2,   Catalase↑,2,   cognitive↑,1,   COX2↓,2,   creat↓,1,   eff↑,2,   eNOS↓,1,   Ferroptosis↓,1,   GlucoseCon↑,1,   GPx↑,1,   GPx4↑,1,   GSH↑,3,   GSSG↓,1,   GSTs↑,1,   GutMicro↑,1,   H2O2↓,1,   hepatoP↑,2,   Hif1a↓,1,   HMGB1↓,1,   HO-1↑,1,   IGF-1↑,1,   IL1β↓,2,   IL6↓,3,   Inflam↓,3,   iNOS↓,1,   IronCh↑,1,   p‑JNK↓,1,   lipid-P↓,2,   MAPK↓,1,   MDA↓,2,   memory↑,1,   MMP↓,1,   MMP↑,2,   MMP2↓,1,   MMP9↑,1,   motorD↓,1,   mTOR↑,1,   neuroP↑,7,   NF-kB↓,2,   NO↓,1,   NRF2↑,1,   p38↓,1,   P450↑,1,   PGE2↓,2,   ROS↓,5,   SOD↑,3,   Src↓,1,   TAC↑,1,   TfR1/CD71↓,1,   Thiols↑,1,   TNF-α↓,2,   VitC↑,1,   VitE↑,1,  
Total Targets: 66

Scientific Paper Hit Count for: neuroP, neuroprotective
9 Rosmarinic acid
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:142  Target#:1105  State#:%  Dir#:%
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