Cphi & P-MEC China Exhibition List展商名单version版本20180116
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The National Drugs List
^ ^ ^ ^ ^[ ^ The National Drugs List Of Syrian Arab Republic Sexth Edition 2006 ! " # "$ % &'() " # * +$, -. / & 0 /+12 3 4" 5 "$ . "$ 67"5,) 0 " /! !2 4? @ % 88 9 3: " # "$ ;+<=2 – G# H H2 I) – 6( – 65 : A B C "5 : , D )* . J!* HK"3 H"$ T ) 4 B K<) +$ LMA N O 3 4P<B &Q / RS ) H< C4VH /430 / 1988 V W* < C A GQ ") 4V / 1000 / C4VH /820 / 2001 V XX K<# C ,V /500 / 1992 V "!X V /946 / 2004 V Z < C V /914 / 2003 V ) < ] +$, [2 / ,) @# @ S%Q2 J"= [ &<\ @ +$ LMA 1 O \ . S X '( ^ & M_ `AB @ &' 3 4" + @ V= 4 )\ " : N " # "$ 6 ) G" 3Q + a C G /<"B d3: C K7 e , fM 4 Q b"$ " < $\ c"7: 5) G . HHH3Q J # Hg ' V"h 6< G* H5 !" # $%" & $' ,* ( )* + 2 ا اوا ادو +% 5 j 2 i1 6 B J' 6<X " 6"[ i2 "$ "< * i3 10 6 i4 11 6! ^ i5 13 6<X "!# * i6 15 7 G!, 6 - k 24"$d dl ?K V *4V h 63[46 ' i8 19 Adl 20 "( 2 i9 20 G Q) 6 i10 20 a 6 m[, 6 i11 21 ?K V $n i12 21 "% * i13 23 b+ 6 i14 23 oe C * i15 24 !, 2 6\ i16 25 C V pq * i17 26 ( S 6) 1, ++ &"r i19 3 +% 27 G 6 ""% i19 28 ^ Ks 2 i20 31 % Ks 2 i21 32 s * i22 35 " " * i23 37 "$ * i24 38 6" i25 39 V t h Gu* v!* 2 i26 39 ( 2 i27 40 B w< Ks 2 i28 40 d C &"r i29 42 "' 6 i30 42 " * i31 42 ":< * i32 5 ./ 0" -33 4 : ANAESTHETICS $ 1 2 -1 :GENERAL ANAESTHETICS AND OXYGEN 4 $1 2 2- ATRACURIUM BESYLATE DROPERIDOL ETHER FENTANYL HALOTHANE ISOFLURANE KETAMINE HCL NITROUS OXIDE OXYGEN PROPOFOL REMIFENTANIL SEVOFLURANE SUFENTANIL THIOPENTAL :LOCAL ANAESTHETICS !67$1 2 -5 AMYLEINE HCL=AMYLOCAINE ARTICAINE BENZOCAINE BUPIVACAINE CINCHOCAINE LIDOCAINE MEPIVACAINE OXETHAZAINE PRAMOXINE PRILOCAINE PREOPERATIVE MEDICATION & SEDATION FOR 9*: ;< " 2 -8 : : SHORT -TERM PROCEDURES ATROPINE DIAZEPAM INJ. -
First Reversals of Cognitive Decline in Alzheimer's Disease and Its
1/12/2017 First Reversals of Cognitive Decline in Alzheimer’sSystems Therapeutics, Disease and its PresidentPrecursors, Obama, MCI and and the End ofSCI Alzheimer’s Disease Dale E. Bredesen, M.D. Augustus Rose Professor Easton Laboratories for Neurodegenerative Disease Research UCLA Founding President, Buck Institute “There is nothing that will prevent, reverse, or slow the progress of Alzheimer’s disease.” “Everyone knows someone who is a cancer survivor; no one knows an Alzheimer’s survivor.” 1 1/12/2017 30,000,000 patients in 2012 3rd leading cause (James, B. D. et al. Contribution of Alzheimer disease to mortality in the United States. Neurology 82, 1045-1050, doi:10.1212/WNL. 0240 (2014) Pres. Obama and NAPA, 2011 160,000,000 patients in 2050 2 1/12/2017 Women at the epicenter of the epidemic •65% of patients •60% of caregivers •More common than breast cancer 0 Cures 3 1/12/2017 Alzheimer’s Disease (AD) Therapeutic Landscape A production APPROVED A aggregation Donepezil (Aricept) A clearance Rivastigmine (Exelon) Tau aggregation/phosph Galantamine (Razadyne) Cholinergic drugs Tacrine (Cognex) Others Memantine (Namenda) PHASE 3 PHASE 2 PHASE 1 Solanezumab ELND005 PBT2 AL-108 GSK933776 NIC5-15 PF04360365 AF102B MABT5102A Bapineuzmab Valproate Bryostatin-1 Nicotinamide Talsaclidine EHT-0202 NP12 ACC001 UB311 Alzemed Antioxidant BMS708163 Lithium AN1792 R1450 Begacestat Semagacestat Statins ABT089 NGF CAD106 V950 PF3084014 AZD3480 SB742457 Flurizan Dimebon E2012 Huperzine-A PRX03140 CTS21166 Rosiglitazone EGCg EVP6124 PUFA MK0752 MEM3454 TTP448 Phenserine CHF5074 PF-04447943 Clinical Trial in AD terminated “Game of Throwns” (243/244) R.I.P. R.I.P. R.I.P. -
Estroquench™ Hormone Specific Formulation™
PRODUCT DATA DOUGLAS LABORATORIES® 08/2014 1 EstroQuench™ Hormone Specific Formulation™ DESCRIPTION EstroQuench™ is a Hormone Specific Formulation™ of ingredients that have documented anti-aromatase activity as well as androgenic adaptogens which support the function of endogenous aromatase inhibitors. Collectively these herbs promote minimal production and function of estrogens, while promoting testosterone function, including optimal sexual function in both genders. This formulation is designed to quench excessive production of estrogens and aberrant functions of them while supporting optimal function of androgens by maintaining the health of androgen producing glands.† Hormone Specific Formulation™ provided by Douglas Laboratories® and formulated by Dr. Joseph J Collins is created to support the optimal function of specific hormones through the use of hormone specific adaptogens, hormone specific agonists and hormone specific functional mimetics. This formulation may be used as part of a hormone health program with dietary and nutrient support. In addition, this formulation may be used by clinicians as an adjuvant to support optimal hormone health in patients who have been prescribed bioidentical hormone therapies. FUNCTIONS Aromatase (a cytochrome P450 enzyme {CYP19}) is the enzyme that controls the conversion of androgens to estrogens. More specifically, aromatase is the enzyme responsible for catalyzing the biosynthesis of androstenedione into estrone, and the biosynthesis of testosterone to estradiol. Estrogens include the broad range of aromatized hormones created form androgens. The specific attribute of estrogens that separate them from progestogens, androgens and corticoids is that estrogens are the only aromatized steroid hormones. Estradiol, the most potent endogenous estrogen, is biosynthesized by aromatization from androgens by aromatase (which is also called estrogen synthase). -
Supplementary Materials Evodiamine Inhibits Both Stem Cell and Non-Stem
Supplementary materials Evodiamine inhibits both stem cell and non-stem-cell populations in human cancer cells by targeting heat shock protein 70 Seung Yeob Hyun, Huong Thuy Le, Hye-Young Min, Honglan Pei, Yijae Lim, Injae Song, Yen T. K. Nguyen, Suckchang Hong, Byung Woo Han, Ho-Young Lee - 1 - Table S1. Short tandem repeat (STR) DNA profiles for human cancer cell lines used in this study. MDA-MB-231 Marker H1299 H460 A549 HCT116 (MDA231) Amelogenin XX XY XY XX XX D8S1179 10, 13 12 13, 14 10, 14, 15 13 D21S11 32.2 30 29 29, 30 30, 33.2 D7S820 10 9, 12 8, 11 11, 12 8 CSF1PO 12 11, 12 10, 12 7, 10 12, 13 D3S1358 17 15, 18 16 12, 16, 17 16 TH01 6, 9.3 9.3 8, 9.3 8, 9 7, 9.3 D13S317 12 13 11 10, 12 13 D16S539 12, 13 9 11, 12 11, 13 12 D2S1338 23, 24 17, 25 24 16 21 D19S433 14 14 13 11, 12 11, 14 vWA 16, 18 17 14 17, 22 15 TPOX 8 8 8, 11 8, 9 8, 9 D18S51 16 13, 15 14, 17 15, 17 11, 16 D5S818 11 9, 10 11 10, 11 12 FGA 20 21, 23 23 18, 23 22, 23 - 2 - Table S2. Antibodies used in this study. Catalogue Target Vendor Clone Dilution ratio Application1) Number 1:1000 (WB) ADI-SPA- 1:50 (IHC) HSP70 Enzo C92F3A-5 WB, IHC, IF, IP 810-F 1:50 (IF) 1 :1000 (IP) ADI-SPA- HSP90 Enzo 9D2 1:1000 WB 840-F 1:1000 (WB) Oct4 Abcam ab19857 WB, IF 1:100 (IF) Nanog Cell Signaling 4903S D73G4 1:1000 WB Sox2 Abcam ab97959 1:1000 WB ADI-SRA- Hop Enzo DS14F5 1:1000 WB 1500-F HIF-1α BD 610958 54/HIF-1α 1:1000 WB pAkt (S473) Cell Signaling 4060S D9E 1:1000 WB Akt Cell Signaling 9272S 1:1000 WB pMEK Cell Signaling 9121S 1:1000 WB (S217/221) MEK Cell Signaling 9122S 1:1000 -
Test Report Comprehensive Hormone Insights™
698814 COMPREHENSIVE HORMONE INSIGHTS™ TEST REPORT Dr. Maximus, N.D. E: [email protected] Date of Collection: P: 403-241-4500 Time of Collection: F: 403-241-4501 Date of Receipt: www.rmalab.com Reported On: CHI Accession: 698814 Healthcare Professional Patient Age: Dr. Maximus, N.D. Date of Birth: Gender: Male F: Relevant Medications Biometrics Curcumin Height (in) : 73 Weight (lb) : 180 BMI : 24 Waist (in) : 35 Hip (in) : 41 CHI Accession: 698814 SUMMARY HMUS01 How to read the graphs LEGEND: 50 66 Sex Steroid Hormones 50 66 Middle third of 33 33 84 reference population Hormone Start of 83 100 80 100 highest 16 Percentile Precursors 16 Percentile third of Sum of Androgens Sum of Estrogens 50 66 reference 0 0 population (T, DHT, α+β androstanediol) Listed in Interp Guide 33 84 End of 100 16 lowest Percentile00 50 66 50 66 third of 33 33 84 reference 0 population Patient’s percentile rank 81 100 95 100 compared to reference 16 Percentile 16 Percentile population (see summary) DHEA + Metabolites Sum of Progesterone Metabolites 0 (DHEA + A + E) 0 α+β Pregnanediol Cortisol Melatonin Oxidative Stress Free Cortisol Profile (ng/mg) 100 50 66 50 66 33 84 33 84 80 64 100 0 100 16 Percentile 16 Percentile 60 6-sulfatoxy 8-Hydroxy-2- 0 Melatonin 0 deoxyguanosine 40 (Overnight) (Overnight) 20 6-sulfatoxymelatonin provides 8-hydroxy-2-deoxyguanosine is Cortisol/Creatinine (ng/mg) insight into melatonin levels. a marker of oxidative stress 0 Morning Dinner Bedtime A B C 50 66 Free cortisol Cortisol Metabolites 33 84 profile is used to provides a general Testosterone Cortisol assess diurnal assessment of 16 100 cortisol rhythm adrenal cortisol 16 Percentile Cortisol production Cortisol Metabolites 0 (α+β THF + THE) Testosterone Cortisol/Testosterone provides insight into relative catabolic (cortisol) and anabolic (testosterone) states. -
Mode of Action
STROKE TBI DEMENTIA Mode of Action Reconnecting Neurons. Empowering for Life. NEW MULTI-MODAL THERAPIES FOR NEUROLOGICAL DISORDERS Sonic hedgehog (Shh) The Sonic Hedgehog (Shh) signalling pathway regulates the development Smoothened of organs including the organization of the brain. For example, the Shh (Smo) Patched (Ptch) activates the Gli complex, which is responsible for the expression of develop- mental genes underpinning neurorecovery and leading to an amplification of natural recovery. Gli Complex Gli Repressor Gli Activator Cerebrolysin activates the Shh pathway1 Cerebrolysin has a promoting effect on neurogenesis and oligodendrogenesis via stimulating the expression of the Shh signalling pathway. Cerebrolysin increases mRNA modulation of Shh and its receptors ‘Patched’ (Ptch) and ‘Smoothened’ (Smo). Shh PTCH Smo 5 * * 3 * 3 4 (n=9) (n=9) *p<0.05 (n=9) *p<0.05 *p<0.05 3 2 2 2 1 1 Fold changes (mean±SE) changes Fold (mean±SE) changes Fold 1 (mean±SE) changes Fold 0 0 0 0 20 0 20 0 20 CERE (µl/ml) CERE (µl/ml) CERE (µl/ml) Figure 1: Cerebrolysin stimulates the expression of the sonic hedgehog signalling pathway components in neural progenitor cells. Graphs show mRNA levels in an in vitro experiment. Studies confirm the important role of the sonic hedgehog pathway in post-stroke brain repair and functional recovery, and suggests the Shh pathway to be a possible target for prolongation of the therapeutic window after stroke.2 MAINTENANCE AND RECOVERY OF THE NEURONAL NETWORK Neurotrophic factors (NTFs) are signaling molecules that maintain, protect, and restore the neuronal network and ensure proper functioning of the brain. -
2018 Apigenin Male Infertility (2).Pdf
Original Article Thai Journal of Pharmaceutical Sciences Apigenin and baicalin, each alone or in low-dose combination, attenuated chloroquine induced male infertility in adult rats Amira Akilah, Mohamed Balaha*, Mohamed-Nabeih Abd-El Rahman, Sabiha Hedya Department of Pharmacology, Faculty of Medicine, Tanta University, Postal No. 31527, El-Gish Street, Tanta, Egypt Corresponding Author: Department of Pharmacology, ABSTRACT Faculty of Medicine, Tanta University, Postal No. 31527, Introduction: Male infertility is a worldwide health problem, which accounts for about 50% of all El-Gish Street, Tanta, Egypt. cases of infertility and considered as the most common single defined cause of infertility. Recently, Tel.: +201284451952. E-mail: apigenin and baicalin exhibited a powerful antioxidant and antiapoptotic activities. Consequently, in [email protected]. the present study, we evaluated the possible protective effect of apigenin and baicalin, either alone or Edu.Eg (M. Balaha). in low-dose combination, on a rat model of male infertility, regarding for its effects on the hormonal assay, testicular weight, sperm parameters, oxidative-stress state, apoptosis, and histopathological Received: Mar 06, 2018 changes. Material and methods: 12-week-old adult male Wister rats received 10 mg/kg/d Accepted: May 08, 2018 chloroquine orally for 30 days to induce male infertility. Either apigenin (30 or 15 mg/kg/d), baicalin Published: July 10, 2018 (100 or 50 mg/kg/d) or a combination of 15 mg/kg/d apigenin and 50 mg/kg/d baicalin received daily -
Mechanisms of Toxic Action of the Flavonoid Quercetin and Its Phase II Metabolites
Mechanisms of toxic action of the flavonoid quercetin and its phase II metabolites Hester van der Woude Promotor: Prof. Dr. Ir. I.M.C.M. Rietjens Hoogleraar in de Toxicologie Wageningen Universiteit Co-promotor: Dr. G.M. Alink Universitair Hoofddocent, Sectie Toxicologie Wageningen Universiteit. Promotiecommissie: Prof. Dr. A. Bast Universiteit Maastricht Dr. Ir. P.C.H. Hollman RIKILT Instituut voor Voedselveiligheid, Wageningen Prof. Dr. Ir. F.J. Kok Wageningen Universiteit Prof. Dr. T. Walle Medical University of South Carolina, Charleston, SC, USA Dit onderzoek is uitgevoerd binnen de onderzoekschool VLAG Mechanisms of toxic action of the flavonoid quercetin and its phase II metabolites Hester van der Woude Proefschrift ter verkrijging van de graad van doctor op gezag van de rector magnificus van Wageningen Universiteit, Prof. Dr. M.J. Kropff, in het openbaar te verdedigen op vrijdag 7 april 2006 des namiddags te half twee in de Aula Title Mechanisms of toxic action of the flavonoid quercetin and its phase II metabolites Author Hester van der Woude Thesis Wageningen University, Wageningen, the Netherlands (2006) with abstract, with references, with summary in Dutch. ISBN 90-8504-349-2 Abstract During and after absorption in the intestine, quercetin is extensively metabolised by the phase II biotransformation system. Because the biological activity of flavonoids is dependent on the number and position of free hydroxyl groups, a first objective of this thesis was to investigate the consequences of phase II metabolism of quercetin for its biological activity. For this purpose, a set of analysis methods comprising HPLC-DAD, LC-MS and 1H NMR proved to be a useful tool in the identification of the phase II metabolite pattern of quercetin in various biological systems. -
Note: the Letters 'F' and 'T' Following the Locators Refers to Figures and Tables
Index Note: The letters ‘f’ and ‘t’ following the locators refers to figures and tables cited in the text. A Acyl-lipid desaturas, 455 AA, see Arachidonic acid (AA) Adenophostin A, 71, 72t aa, see Amino acid (aa) Adenosine 5-diphosphoribose, 65, 789 AACOCF3, see Arachidonyl trifluoromethyl Adlea, 651 ketone (AACOCF3) ADP, 4t, 10, 155, 597, 598f, 599, 602, 669, α1A-adrenoceptor antagonist prazosin, 711t, 814–815, 890 553 ADPKD, see Autosomal dominant polycystic aa 723–928 fragment, 19 kidney disease (ADPKD) aa 839–873 fragment, 17, 19 ADPKD-causing mutations Aβ, see Amyloid β-peptide (Aβ) PKD1 ABC protein, see ATP-binding cassette protein L4224P, 17 (ABC transporter) R4227X, 17 Abeele, F. V., 715 TRPP2 Abbott Laboratories, 645 E837X, 17 ACA, see N-(p-amylcinnamoyl)anthranilic R742X, 17 acid (ACA) R807X, 17 Acetaldehyde, 68t, 69 R872X, 17 Acetic acid-induced nociceptive response, ADPR, see ADP-ribose (ADPR) 50 ADP-ribose (ADPR), 99, 112–113, 113f, Acetylcholine-secreting sympathetic neuron, 380–382, 464, 534–536, 535f, 179 537f, 538, 711t, 712–713, Acetylsalicylic acid, 49t, 55 717, 770, 784, 789, 816–820, Acrolein, 67t, 69, 867, 971–972 885 Acrosome reaction, 125, 130, 301, 325, β-Adrenergic agonists, 740 578, 881–882, 885, 888–889, α2 Adrenoreceptor, 49t, 55, 188 891–895 Adult polycystic kidney disease (ADPKD), Actinopterigy, 223 1023 Activation gate, 485–486 Aframomum daniellii (aframodial), 46t, 52 Leu681, amino acid residue, 485–486 Aframomum melegueta (Melegueta pepper), Tyr671, ion pathway, 486 45t, 51, 70 Acute myeloid leukaemia and myelodysplastic Agelenopsis aperta (American funnel web syndrome (AML/MDS), 949 spider), 48t, 54 Acylated phloroglucinol hyperforin, 71 Agonist-dependent vasorelaxation, 378 Acylation, 96 Ahern, G. -
Workbook Psychiatry and Narcology
Kharkiv National Medical University Department of Psychiatry, Narcology and Medical Psychology WORKBOOK MANUAL FOR INDIVIDUAL WORK FOR MEDICAL STUDENTS PSYCHIATRY AND NARCOLOGY (Part 2) Student ___________________________________________________________ Faculty _________________________________________________________ Course _________________ Group _____________________________________ Kharkiv 2019 Затверджено вченою радою ХНМУ Протокол №5 від 23.05.2019 р. Psychiatry (Part 2) : workbook manual for individual work of students / I. Strelnikova, G. Samardacova, К. Zelenska – Kharkiv, 2019. – 103 p. Копіювання для розповсюдження в будь-якому вигляді частин або повністю можливо тільки з дозволу авторів навчального посібника. CLASS 7. NEUROTIC DISORDERS. CLINICAL FORMS. TREATMENT AND REHABILITATION. POSTTRAUMATIC STRESS DISORDER. TREATMENT AND REHABILITATION. Psychogenic diseases are a large and clinically varied group of diseases resulting from an effect of acute or long-term psychic traumas, which manifest themselves by both mental and somatoneurological disorders and, as a rule, are reversible. Psychogenic diseases are caused by a psychic trauma, i.e. some events which affect significant aspects of existence of the human being and result in deep psychological feelings. These may be subjectively significant events, i.e. those which are pathogenic for the majority of people. Besides, the psyche may be traumatized by conventionally pathogenic events, which cause feelings in an individual because of his peculiar hierarchy of values. Unfavorable psychogenic effects on the human being cause stress in him, i.e. a nonspecific reaction at the physiological, psychological and behavioural levels. Stress may exert some positive, mobilizing influence, but may result in disorganization of the organism activity. The stress, which exerts a negative influence and causes various disturbances and even diseases, is termed distress. Classification of neurotic disorders I. -
Drug Name Plate Number Well Location % Inhibition, Screen Axitinib 1 1 20 Gefitinib (ZD1839) 1 2 70 Sorafenib Tosylate 1 3 21 Cr
Drug Name Plate Number Well Location % Inhibition, Screen Axitinib 1 1 20 Gefitinib (ZD1839) 1 2 70 Sorafenib Tosylate 1 3 21 Crizotinib (PF-02341066) 1 4 55 Docetaxel 1 5 98 Anastrozole 1 6 25 Cladribine 1 7 23 Methotrexate 1 8 -187 Letrozole 1 9 65 Entecavir Hydrate 1 10 48 Roxadustat (FG-4592) 1 11 19 Imatinib Mesylate (STI571) 1 12 0 Sunitinib Malate 1 13 34 Vismodegib (GDC-0449) 1 14 64 Paclitaxel 1 15 89 Aprepitant 1 16 94 Decitabine 1 17 -79 Bendamustine HCl 1 18 19 Temozolomide 1 19 -111 Nepafenac 1 20 24 Nintedanib (BIBF 1120) 1 21 -43 Lapatinib (GW-572016) Ditosylate 1 22 88 Temsirolimus (CCI-779, NSC 683864) 1 23 96 Belinostat (PXD101) 1 24 46 Capecitabine 1 25 19 Bicalutamide 1 26 83 Dutasteride 1 27 68 Epirubicin HCl 1 28 -59 Tamoxifen 1 29 30 Rufinamide 1 30 96 Afatinib (BIBW2992) 1 31 -54 Lenalidomide (CC-5013) 1 32 19 Vorinostat (SAHA, MK0683) 1 33 38 Rucaparib (AG-014699,PF-01367338) phosphate1 34 14 Lenvatinib (E7080) 1 35 80 Fulvestrant 1 36 76 Melatonin 1 37 15 Etoposide 1 38 -69 Vincristine sulfate 1 39 61 Posaconazole 1 40 97 Bortezomib (PS-341) 1 41 71 Panobinostat (LBH589) 1 42 41 Entinostat (MS-275) 1 43 26 Cabozantinib (XL184, BMS-907351) 1 44 79 Valproic acid sodium salt (Sodium valproate) 1 45 7 Raltitrexed 1 46 39 Bisoprolol fumarate 1 47 -23 Raloxifene HCl 1 48 97 Agomelatine 1 49 35 Prasugrel 1 50 -24 Bosutinib (SKI-606) 1 51 85 Nilotinib (AMN-107) 1 52 99 Enzastaurin (LY317615) 1 53 -12 Everolimus (RAD001) 1 54 94 Regorafenib (BAY 73-4506) 1 55 24 Thalidomide 1 56 40 Tivozanib (AV-951) 1 57 86 Fludarabine -
(Apigenin, Luteolin, Chrysin) and Their Importance for Health
Mellifera 2020, 20(1):16-27 MELLIFERA REVIEW ARTICLE Flavones (Apigenin, Luteolin, Chrysin) and Their Importance for Health Fatma Özsel ÖZCAN1*, Ozan ALDEMİR2, Bülent KARABULUT3 1Beykoz Üniversity, Faculty of Art and Design, Department of Gastronomy and Culinary Arts, İstanbul, Turkey 2Ege University Faculty of Medicine, Department of Biochemistry, İzmir, TURKEY 3Ege University Faculty of Medicine, Department of Oncology, İzmir, TURKEY * Corresponding author e-mail: [email protected] Received: 14th March, 2020; accepted: 4th May, 2020; published: 29th June, 2020 A B S T R A C T It has been shown in recent years that foods called functional foods may protect against certain types of cancer, cardiovascular diseases and cognitive dysfunctions. In the studies performed, the flavonoids (apigenin, chrysin, luteolin) which are subclass of flavonoids have been shown to have antioxidant, antiinflammatory, antiallergic, neuroprotective and cardioprotective effects and it is presented as the current treatment method in the treatment of some diseases. The structure function, nutritional resources and potential therapeutic properties of the flavones, which are also used as supplement in the compost, have been studied. The purpose of this review is to evaluate the therapeutic effects of flavones in certain diseases. The positive effect of 16 flavones on health can be proven in many experimental studies and can be proven in the long run. Keywords: Functional nutrients, flavones, apigenin, luteolin, chrysin Introduction Polyphenolic flavonoids are among the affected by factors such as plant species, wide variety of phytochemicals found in the environment, genetics, light, maturity, human diet. Current studies reveal that harvest [3]. Flavones, a subset of dietary flavonoids are inversely related to flavonoids, form glycosylation and contain many cancers and age-related diseases [1].