Epitalon Nasal Spray

Epitalon Nasal Spray
Paub meej:
1. General Specification (hauv Tshuag)
(1) API (Ntshiab hmoov)
(2) Cov ntsiav tshuaj
(3) Txhaj tshuaj
(4) Qhov ntswg qhov ntswg
(5) Capsule
2.Customization:
Peb yuav sib tham tus kheej, OEM / ODM, Tsis muaj hom, rau kev tshawb nrhiav kev ruaj ntseg nkaus xwb.
Internal Code: KP-1-7/005
Epitalon CAS 307297-39-8
Kev tshuaj xyuas: HPLC, LC-MS, HNMR
Kev them nyiaj yug Technology: R&D Dept.-4
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Hauj lwm lawm
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Epitalon nasal sprayyog ib qho hluavtaws pineal tetrapeptide ntseeg tias muaj peev xwm tseem ceeb hauv kev tiv thaiv kabmob kheesxaws. Nws cov txiaj ntsig tseem ceeb nyob hauv nws lub peev xwm los cuam tshuam qhov tshwm sim ntawm cov qog nqaij hlav, txo cov qog metastasis, thiab txuas ntxiv cov qog nqaij hlav - dawb ciaj sia. Cov kev tshawb fawb tam sim no qhia tau hais tias cov khoom siv peptide no ua rau nws cov teebmeem los ntawm ntau yam kev ua haujlwm lom neeg, suav nrog kev ua kom telomerase kev ua haujlwm, tswj cov kev qhia ntawm cov noob ntsig txog kev loj hlob ntawm tes thiab apoptosis, txhim kho kev tiv thaiv antioxidant, thiab hloov kev tiv thaiv kab mob. Cov teebmeem no sib sau ua ke ua lub hauv paus theoretical rau nws lub luag haujlwm hauv kev cuam tshuam hauv kev pib thiab kev loj hlob ntawm cov qog.

Nrog rau kev mob qog noj ntshav nce zuj zus, qhov tseem ceeb ntawm cov tshuaj tiv thaiv tau dhau los ua qhov tseem ceeb. Tam sim no, kev tshawb fawb txog qhov no tau nce qib los ntawm kev tshawb fawb yooj yim mus rau kev siv tshuaj kho mob, ua tib zoo saib xyuas nws qhov ua tau thiab kev nyab xeeb raws li tus neeg sawv cev tshuaj tiv thaiv rau cov qog. Nyob rau hauv lub neej yav tom ntej, tetrapeptide no tuav cov lus cog tseg raws li lub tswv yim tshiab kev tiv thaiv kab mob lom, muab kev xaiv rau cov tib neeg noj qab haus huv lossis siab - pab pawg muaj kev pheej hmoo los txo lawv txoj kev pheej hmoo ntawm qog hlav, yog li qhib txoj hauv kev tshiab hauv kev tiv thaiv kab mob qog noj ntshav.

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Thaum tsim cov tshuaj no ua cov tshuaj tsuag rau kev tiv thaiv qog, piv rau kev txhaj tshuaj ib txwm siv, cov tshuaj tsuag yog nqus ncaj qha los ntawm qhov ntswg / qhov ncauj mucosa yam tsis muaj qhov mob ntawm koob. Qhov no ua rau nws tsim nyog rau ntev - siv kev tiv thaiv nyob rau hauv cov pej xeem uas muaj kev pheej hmoo ntawm cov qog nqaij hlav, hais txog qhov teeb meem ntawm kev ua tsis zoo uas cuam tshuam nrog cov tshuaj txhaj tshuaj. Ntxiv mus, nws cov mucosal absorption yog sai thiab muaj kev txhim kho lub hom phiaj. Muab cov nplua nuj capillary thiab lymphatic networks hauv qhov ntswg thiab qhov ncauj mucosa, qhovEpitalon nasal spraytuaj yeem nkag mus rau hauv cov hlab ntsha ncaj qha los ntawm cov mucosa, hla kev zom zaub mov thiab lub siab ua ntej - dhau los, ua rau muaj qhov pib sai dua. Tsis tas li ntawd, kev tswj xyuas qhov ntswg tuaj yeem ua ncaj qha rau hauv nruab nrab lub hom phiaj xws li pineal caj pas, uas tuaj yeem txhim kho nws cov txiaj ntsig tseem ceeb hauv kev tswj hwm telomerase thiab muab cov txiaj ntsig antioxidant.

Cov txheej txheem tshuaj tsuag tso cai rau kev tswj xyuas meej ntawm ib zaug - kev tswj hwm koob tshuaj, txo cov kev hloov pauv hauv cov tshuaj concentration hauv lub cev. Qhov no yuav pab txo qis cov kev pheej hmoo xws li telomerase overactivation thiab cell immortalization uas yuav tshwm sim los ntawm ntev -lub sij hawm, siab - koob tshuaj, yog li ua kom zoo dua qub nrog kev nyab xeeb ntawm kev tiv thaiv qog.

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Ua kom genomic stability, lub hauv paus tiv thaiv kab mob qog noj ntshav

Telomeres yog cov txheej txheem tiv thaiv ntawm qhov kawg ntawm eukaryotic chromosomes, thiab lawv qhov ntev yuav maj mam txo nrog kev faib ntawm tes. Thaum telomeres luv luv mus rau qhov tseem ceeb, lawv tuaj yeem ua rau genomic instability txheej xwm xws li chromosome breakage, fusion, thiab rearrangement, uas kuj yog cov tseem ceeb tsav tsheb ntawm malignant transformation nyob rau hauv hlwb.
Epitalon txoj cai ntawm telomerase yog tus cwj pwm los ntawm kev ua kom nruab nrab thiab lub hom phiaj meej. Nws lub luag haujlwm hauv kev thaiv cov kab mob carcinogenesis tuaj yeem ua tiav los ntawm peb txoj hauv kev tseem ceeb hauv qab no:

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Targeted Activation ntawm Telomerase Reverse Transcriptase (TERT)

TERT yog lub hauv paus catalytic subunit ntawm telomerase complex, thiab nws cov transcriptional thiab translational theem ncaj qha txiav txim telomerase kev ua. Cov kev tshawb fawb tsiaj tau lees paub tias cov tshuaj tuaj yeem txhim kho cov qib mRNA transcription thiab cov protein qhia ntawm TERT gene hauv cov pob txha pob txha thiab cov hlwb mammary epithelial, yog li ua kom cov catalytic muaj nuj nqi ntawm telomerase thiab txhawb kev ruaj ntseg thiab kev puas tsuaj ntawm telomere ntev. Hauv HER-2/neu transgenic nas qauv, qhov tshwm sim ntawm chromosomal aberrations nyob rau hauv cov pob txha pob txha hlwb ntawm Epitalon-kho pab pawg yog 17.1% qis dua li ntawm pawg tswj, nws zoo txo ​​genomic puas tsuaj los ntawm telomere dysfunction.

Kev ncua ntawm Cellular Replicative Senescence thiab txo qis kev pheej hmoo ntawm kev loj hlob

Cellular senescence feem ntau yog categorized rau replicaative senescence thiab kev nyuaj siab-induced senescence, nrog kev loj hlob telomere shortening yog tus tseem ceeb tsav tsheb ntawm replicaative senescence. Los ntawm stabilizing telomere ntev, Epitalon tuaj yeem ncua qhov pib ntawm replicaative senescence nyob rau hauv ib txwm somatic hlwb, yog li tiv thaiv qhov txawv txav ntawm lub senescence -sociated secretory phenotype (SASP). SASP tso tawm ntau cov tshuaj bioactive xws li inflammatory mediators thiab matrix metalloproteinases, uas tuaj yeem txhawb kev hloov pauv tsis zoo hauv cov hlwb ib puag ncig. Nws yog ib qho tseem ceeb uas yuav tsum tau hais txog tias cov txheej txheem kev tswj hwm no nthuav tawm qhov tseeb ntawm tes, ua haujlwm ntawm lub cev somatic nkaus xwb yam tsis muaj kev txhim kho telomerase kev ua haujlwm hauv cov hlwb uas twb muaj lawm. Qhov no ua tau zoo zam qhov kev pheej hmoo ntawm "txhawb cov qog cell immortalization."

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Txo Chromosomal Instability (CIN)

Genomic instability yog ib qho tseem ceeb ntawm cov qog nqaij hlav malignant, thiab telomere dysfunction yog thawj qhov ua rau chromosomal instability (CIN). Qhov no ua tau zoo txo ​​qhov zaus ntawm cov xwm txheej txawv txav xws li chromosome breakage, translocation, thiab deletion, txo qis qhov tshwm sim ntawm qog suppressor gene inactivation thiab oncogene activation. Qhov no, nyob rau hauv lem, thaiv cov txheej txheem ntawm malignant transformation ntawm thawj theem ntawm carcinogenesis.

 

Epitalon zoo thiab meej tswj lub voj voog ntawm tes thiab apoptosis

Telomeres yog cov txheej txheem tiv thaiv ntawm qhov kawg ntawm eukaryotic chromosomes, thiab lawv qhov ntev yuav maj mam txo nrog kev faib ntawm tes. Thaum telomeres luv luv mus rau qhov tseem ceeb, lawv tuaj yeem ua rau genomic instability txheej xwm xws li chromosome breakage, fusion, thiab rearrangement, uas kuj yog cov tseem ceeb tsav tsheb ntawm malignant transformation nyob rau hauv hlwb.

(I) Inhibition ntawm Anti-Apoptotic Protein Bcl-2 Kev Qhia:

 

 

Bcl-2 tsev neeg cov proteins yog ib tsev neeg tseem ceeb molecular tswj cov mitochondria-txoj kev kho apoptosis. Kev tsis txaus ntseeg ntau dhau ntawm cov tshuaj tiv thaiv -apoptotic protein Bcl-2 yog ib qho tseem ceeb ntawm cov tshuaj molecular hauv kev loj hlob thiab kev loj hlob ntawm ntau yam qog nqaij hlav malignant. Bcl-2 feem ntau ua haujlwm los ntawm stabilizing mitochondrial membrane muaj peev xwm thiab inhibiting qhov qhib ntawm mitochondrial permeability hloov pore (mPTP), yog li tiv thaiv kev tso tawm ntawm cytochrome C los ntawm mitochondria rau hauv cytoplasm. Qhov no tom qab inhibits qhov ua kom ntawm caspase tsev neeg ntawm cov proteins thiab thaum kawg thaiv qhov pib ntawm qhov kev pab cuam apoptosis. Cov kev qhia txawv txav no tso cai rau DNA puas hlwb txawv txav lossis cov qog nqaij hlav qog nqaij hlav ntxov ntxov kom tsis txhob muaj apoptosis, ua rau lawv muaj sia nyob thiab sib sau ua ke hauv lub cev. Cov hlwb no maj mam kis tus kab mob malignant phenotypes xws li ntxeem tau thiab metastasis, nws thiaj li tsim mus rau cov qog nqaij hlav malignant.

Epitalon nasal spraytuaj yeem txo qis mRNA qhia theem ntawm Bcl-2 noob los ntawm kev hloov kho nws cov txheej txheem kev hloov pauv, yog li txo cov synthesis ntawm Bcl-2 protein. Qhov no cuam tshuam qhov sib npaug ntawm apoptosis thiab kev loj hlob, tshem tawm nws cov nyhuv inhibitory ntawm txoj hauv kev mitochondrial apoptosis, thiab txhawb kev pib ntawm apoptosis thaum ntxov -cov qog nqaij hlav qog noj ntshav, tso cai rau lawv tshem tawm ntawm lub cev. Cov txheej txheem no thaiv cov qog nqaij hlav ntawm theem nrab ntawm carcinogenesis. Hauv C3H / Nws nas (tus qauv qog nqaij hlav tsis zoo), cov kev sim cuam tshuam tau lees paub tias ob qho tib si Bcl-2 protein thiab mRNA qhia qib hauv cov qog nqaij hlav ntawm pawg Epitalon-kho tau qis dua cov hauv pawg tswj hwm. Lub caij no, qhov kev faib ua feem ntawm cov hlwb apoptotic hauv cov qog nqaij hlav tau nce 2-3 zaug piv rau pawg tswj hwm. Cov ntaub ntawv sim no ncaj qha siv cov txiaj ntsig tshwj xeeb ntawm nws hauv kev tiv thaiv qog nqaij hlav thiab kev tawm tsam los ntawm inhibiting Bcl-2 qhia thiab txhawb nqa apoptosis ntawm cov qog nqaij hlav ntxov ntxov. Cov txheej txheem no tsom tag nrho rau kev tshem tawm cov qog nqaij hlav cancer thiab tsis cuam tshuam nrog kev tswj hwm ntawm senescence nyob rau hauv ib txwm cell.

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(II) Txhim kho qhov kev nthuav qhia ntawm DNA Kho Genes:

 

DNA kev puas tsuaj yog ib qho tseem ceeb pib qhov tseem ceeb hauv malignant cellular transformation. Sab nraud stimuli xws li oxidative kev nyuaj siab thiab ionizing hluav taws xob tuaj yeem yooj yim ua rau muaj qhov txawv txav hauv cellular DNA, suav nrog ob npaug -strand so, puag kev puas tsuaj, thiab lub hauv paus tsis sib haum. Yog tias cov kev puas tsuaj no tsis kho raws sijhawm, kev hloov pauv ntawm cov noob tuaj yeem sib sau ua ke, ua rau cov qog nqaij hlav qog tsis ua haujlwm thiab ua kom oncogene, yog li tsav cov hlwb mus rau ib qho phenotype malignant. Epitalon tuaj yeem txhim kho qhov kev qhia ntawm ntau qhov tseem ceeb DNA kho cov noob los ntawm kev hloov kho DNA kho -txog txoj kev taw qhia. Cov no suav nrog cov noob kho tseem ceeb xws li BRCA1, ATM, thiab PARP1, txhua tus ua lub luag haujlwm tseem ceeb hauv cov txheej txheem kho DNA puas: BRCA1 feem ntau koom nrog kev kho homologous recombination ntawm DNA ob -strand so, raug lees paub thiab khi rau ob npaug {-, kev nrhiav neeg ua haujlwm, thiab kev sib koom ua ke ntawm cov protein. ua kom tiav kev kho cov DNA puas.

Lub ATM gene ua raws li "sensor molecule" rau DNA puas, tam sim ntawd paub txog DNA puas cov cim thiab pib kho cov kab hauv qab thaum tswj hwm lub voj voog ntawm tes kom tso sijhawm rau kho DNA. PARP1 feem ntau koom nrog hauv kev kho DNA ib zaug xwb-strand breaks thiab base puas, txo cov noob kev hloov pauv los ntawm kev puas tsuaj.By upregulating lub mRNA thiab protein qhia theem ntawm cov kho cov noob, Epitalon ho txhim kho DNA puas kho lub peev xwm ntawm ib txwm somatic hlwb thiab ntxov-theem puas hlwb, accelerates kho cov txheej txheem ntawm cov muccum ntawm cov DNA puas, accelerates kho cov txheej txheem ntawm muccum. Qhov tshwm sim ntawm oncogene activation thiab qog suppressor gene inactivation. Cov txheej txheem no txo ​​qhov muaj feem ntawm cov qog loj hlob los ntawm thawj theem ntawm carcinogenesis.

 

Saib rau yav tom ntej ntawm Epitaron

Nws yog tsim nyog sau cia tias lub peev xwm ntawmEpitalon nasal sprayHauv kev tiv thaiv qog noj ntshav tsis yog tsuas yog nyob ntawm nws ntau- lub hom phiaj molecular mechanisms- xws li inhibiting kev qhia ntawm cov tshuaj tiv thaiv -apoptotic protein Bcl-2, txhawb kev apoptosis ntawm ntxov- theem mob qog noj ntshav, txhim kho DNA kho, thiab stabilizing cov genome ntawm {7} tab sis nyob rau hauv cov genome. txoj kev xa khoom tshiab. Txoj kev uas tsis yog- qhov ntswg qhov ntswg lossis qhov ncauj tshuaj tua kab mob muaj txiaj ntsig zoo dua li kev txhaj tshuaj ib txwm muaj- raws li kev xa khoom. Cov qauv no tso cai rau kev nqus ncaj qha thiab thauj cov tshuaj los ntawm mucosal epithelial hlwb, zam qhov mob thiab kev pheej hmoo kis mob hauv zos cuam tshuam nrog kev txhaj tshuaj. Nws kuj tseem ua kom yooj yim rau cov txheej txheem tswj hwm, tso cai rau tus kheej - kev tswj hwm yam tsis muaj kev pab los ntawm cov kws kho mob. Qhov no ua tau zoo nrog cov kev xav tau ntawm cov neeg muaj kev pheej hmoo siab uas yuav tsum tau siv tshuaj tiv thaiv ntev - cov tshuaj tiv thaiv ntev, hauv paus ntsiab lus ntawm qhov teeb meem tseem ceeb ntawm kev noj tshuaj tsis zoo rau lub sijhawm ntev los ntawm cov txheej txheem cumbersome thiab cov neeg mob siab ntev ntawm cov tshuaj formulations.

Saib tom ntej, raws li kev tshawb fawb ntawm cov txheej txheem ntawm nws txuas ntxiv mus tob zuj zus thiab qhov tseem ceeb ntawm cov qauv tshuaj tsuag -xws li ntau npaum li cas, kev nqus tau zoo, thiab ntev -lub sij hawm kev nyab xeeb- tau ua kom zoo dua ntxiv, muaj peev xwm los ua ke qhov no nrog cov tshuaj ntsuam genetic testing thev naus laus zis rau qhov tseeb, stratified interventions targeting tej pawg neeg siab 7} xws li {2} overexpression los yog tsev neeg qog susceptibility. Qhov no tuaj yeem nqa qhov yooj yim thiab lub hom phiaj tiv thaiv lub tswv yim rau hauv kev kho mob. Tsis tas li ntawd, cov kev tshawb fawb yav tom ntej tuaj yeem tshawb nrhiav kev sib xyaw ua ke ntawm kev siv tshuaj tsuag nrog cov tshuaj immunomodulators qis. Los ntawm kev sib koom ua ke txhim kho apoptosis induction thiab kev tiv thaiv kev tiv thaiv kev ua haujlwm, kev tiv thaiv qog nqaij hlav tuaj yeem txhim kho ntxiv. Txoj hauv kev no muab cov kev daws teeb meem tshiab thiab siv tau ntau dua los txo qhov tshwm sim ntawm cov qog nqaij hlav, ua rau muaj kev hloov pauv hauv kev tswj mob qog noj ntshav los ntawm "kev kho mob" mus rau "kev tiv thaiv nquag."

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