GDF-8 (Myostatin) 1Mg rau CASBEBINGDING CAS: 271597-12-7

Dab tsi yog anostatin (gdf-8)? Molecular ntsuas kub

Dab Neeg Xwm:Ib tug tswv cuab ntawm kev hloov pauv kev loj hlob - beta (tgf -}) superfamily ntawm cov proteining.

Source Source:Tseem ua synthesized thiab zais los ntawm cov leeg pob txha hlwb (myocytes) lawv tus kheej.

● Mechanism:Muaj nuj nqi raws li lub autocrine / Paracrine signaling molecule. Nws khi rau ib qho kev sib tw ntawm cov receptors ntawm cov leeg nqaij hlwb (feem ntau {actor- actriib, tom qab ntawv nrhiav hom kuv receptors zoo li Alk4 / 5).

Ub Pib teeb liab Transduction:Qhov no khi triggers ib lub ntsej muag hluav taws xob phosporhlation cascade (koom nrog smad protein, tshwj xeeb smad2 / 3). Ua kom smad undlexes kev txhais ua rau lub nucleus.

Kev nqis tes ua nyob rau hauv nucleus:Tsis pub dhau lub nucleus, cov smad cov complexes nrog cov DNA tshwj xeeb thiab co}}} yam kom tswj cov noob.

Nrag thawj los:

○ Inhibition ntawm myoblast cov lus qhia:Suppresses Lub Tuam Txhab Satellite (Cov leeg qia hlwb), txwv lub pas dej ntawm cov hlwb muaj rau kev ua leeg nqaij thiab kev loj hlob.

○ Inhibition ntawm myoblast sib txawv:Hinders lub tiav ntawm lub hlwb ntawm satellite thiab myobblasts rau hauv cov leeg nqaij tshiab (Myotubes).

Kev tsim tawm ntawm cov protein degradation:Upregulates cov ntsiab lus tseem ceeb ntawm Ubiquitin - proteasome system (piv txwv li txoj kev ua cov nqaij protein sib tsoo (atrophy).

○ Tsis ncaj:Modulates lwm cov phiajcim pathwpressing (piv txwv li, kev txhawb nqa AKT / MTOR PATHAYWATION), ntxiv tilting qhov sib npaug deb ntawm cov leeg protein synthesis.

Lub tswv yim ntawm qhov yooj yim "1mg txhaj tshuaj" vahtly oversimplifies qhov kev sib tw. Kev incribition uas yuav tsum tau siv cov cuab yeej muaj tseeb:

1.Target tshwj xeeb:Yuav tsum xaiv block Myostatin (gdf - 8) uas muaj kev cuam tshuam nrog lwm cov txheej txheem (BMPs) Tsis yog feem tshwj xeeb ua rau cov kev mob tshwm sim hnyav.

2.bioavailability & stability:Yuav tsum muaj tus me nyuam me nyuam ua kom cov neeg inhititor tau nce mus txog nws cov phiaj xwm kev ua kom zoo thiab muaj kev cuam tshuam ntev rau kev cuam tshuam rau kev ua haujlwm. Yooj yim peptrides demrade sai.

3.pone:Xav tau high binding affinity rau cov nyhuv sib tw nrog endogenous myostatin rau actriib receptors.

4.Delivate tshuab:Yuav inoretically koom nrog:

○ Cov tshuaj tiv thaiv monoclonal (Mabs):Cov kws ua haujlwm tsim cov tshuaj tiv thaiv kab mob tshwj xeeb khi thiab nruab nrab ntawm cov kab mob uas tsis ua tiav rau cov kab mob uas tsis txaus siab vim muaj kev phom sij / muaj kev nyab xeeb).

○ Soluble recoror decoys:Recombiny Proteins Mimicking Dov Extracellular Sau ntawm Actriib, khi Myostatin nyob rau hauv cov hlab ntshav ua ntej nws mus txog kev txhawj xeeb txog kev tiv thaiv kev nyab xeeb xws li los ntshav).

○ Gene Silencing:Cov thev naus laus zis zoo li Antisens OligonucleAs (Asos) lossis Kev cuam tshuam RNA los tiv thaiv cov tshuaj yauv ua kom tiv thaiv tau ntawm MRNA. Cov txuj ci siab heev thiab ntev-} sij hawm kev nyab xeeb tsis paub.

○ Noob eding:Kev knockout tas mus li ntawm MSTN Gene (piv txwv li, Crispr - Cas9). Kev coj ncaj ncees thiab muaj peev xwm kev phom sij sab nraud kho cov mob hnyav.

Cov kev hais lus tsis txaus siab nyob rau hauv kev kov yeej kev txwv caj ces caj ces:

1.hyperplasia -} tsav huab cua:Tsis Zoo Li Solteroids feem ntau txhawb hypertrophy (txhim kho cov fibers uas twb muaj lawm), Myostatin inhibitionyuavtheoretically txhawbkev tu tub- qhov tsim ntawmtshiabCov leeg nqaij los ntawm lub tshuab ua haujlwm ntawm lub satellite. Qhov no sawv cev rau lub fundamentally sib txawv mechanism rau huab hwm loj.

2.Accelerated rov qab:Los ntawm kev txhim kho lub satellite cell kev koom tes, cov leeg kho cov post - kev cob qhiayuavUa kom sai dua sai dua, tso cai ntau zaus, kev cob qhia kev cob qhia kev cob qhia kev kawm ntau.

3.reded furigability:Qee cov tsiaj cov kev tshawb fawb qhia txog cov leeg ua kom zoo dua, muaj feem cuam tshuam rau cov leeg nqaij lwj (nce cov roj ntsha) lossis metabolic efficiency. Tib neeg txhais lus yog speculative.

4. Koj cov toj noataus:Rau cov neeg ncaws pob uas nyob ze lawv cov caj ces los ntawm cov txheej txheem pa, myostatin inhibitiontej zaummuab txoj hauv kev tshiab rau kev nce ntxiv.

5. "Zoo" Cov Nqaij:Lubyim Condplasiayuavtheoretically ua rau cov leeg loj hlob nrog cov kev sib txawv uas muaj peev xwm sib txawv piv rau hypertrophy {}}} heev ntawm kev xav.

1.Unproven kev ua tau zoo hauv kev noj qab haus huv tib neeg:Txhua lub tsev kho mob sim ua cov tshuaj myostatin tau tsom rau cov leeg nqaij -}}} Cov kab mob uas nkim sij hawm (MD, Cancerenia). Cov txiaj ntsig tau ua tsis txaus siab, ua tsis tau txais txiaj ntsig zoo txawm tias qee qhov loj nce ntxiv. Kev ua tau zoo nyob rau hauvtwb noj qab nyob zoo, kawmCov tib neeg yog tsis paub kiag li thiab yuav nyuaj dua kom ua tiav. Nce yuav yog marginal.

2.Txoj kev txhawj xeeb txog kev nyab xeeb:

○ Tendon & Lainent qaug zog:Cov leeg loj hlobtsis muajProportional ntxiv ntawm cov ntaub so ntswg sib txuas yog daim ntawv qhia rau kev puas tsuaj rau kev puas tsuaj (tawg). Myescatin plays lub luag haujlwm hauv kev loj hlob. Inhibitors tau ua rau cov teeb meem rau cov tsiaj hauv cov tsiaj kev kawm thiab qee qhov kev sim siab.

○ Teeb meem mob plawv:Lub plawv mob (myocardium) qhia cov actriib receptors. Tsis -}} Tshwj Xeeb} Tshwj xeeb inhibitors thaiv lwm cov actriib ligands (zoo li cov tub rog ua kom zoo thiab telangiectels (dilated cov ntshav) hauv kev sim siab (ace-031). Qhov tshwj xeeb yog qhov tseem ceeb thiab nyuaj.

○ Tsis muaj peev xwm ua tau zoo:Tgf -}} superfamily cov tswv cuab tswj cov metabolism thiab rog cia. Kev cuam tshuam kev cuam tshuam yuav ua rau cov tshuaj insulin tsis kam, hloov cov nqaij qaib cov ntaub ntawv, lossis kev npaj ua rog.

○ Cov kev tawm tsam tiv thaiv kab mob:Cov neeg sawv cev roj ntsha (Mabs, soluble receptors) tuaj yeem tiv thaiv kev tiv thaiv kab mob (}

○ Ntev ntev- Tod tsis paub:Qhov cuam tshuam ntawm kev txhawb nqa inhibition ntau xyoo lossis xyoo? Cuam tshuam rau kev laus? Kev pheej hmoo mob cancer kev ntsuas? Kiag li tsis paub kiag li.

3.Tsis "1mg" cov khoom muaj:Tsis muaj cov tshuaj ntsiav - qib, qauv "gdf-8 / myostatin 1mg" vial muaj. Txhua yam khoom lag luam ua lag luam li yog:

○ Kev tshawb fawb tshuaj (RC):Cov chaw tsis paub meej, purity / cov ntsiab lus tsis paub, muaj peev xwm paug, tsim hauv cov qauv tsis muaj cai nrog cov qauv kev nyab xeeb.

○ Ib tus kws txuj ci dag:Ua kom tiav lossis muaj cov khoom tsis paub / tsis muaj kev phom sij (muaj peev xwm txaus ntshai).

4.Lab nrho & cov xwm txheej zoo:Myostatin Inhibitors tsis tau pom zoo rau kev ua tau zoo ua tiav. Kev siv yuav tsim kho doping, ua rau kev sib tw bans. Tau txais lawv muaj feem cuam tshuam cov kev lag luam dub / grey.

Ceeb Toom:Ntu no yog cov kev ua haujlwm ntawm theoretical extrapolation raws li cov chaw kuaj mob tsis txaus ntseeg rauKab mob hais. Nws tsis yog sawv cev kev nyab xeeb lossis ua haujlwm zoo.

● Dosage:Cov kev sim kho mob siv Mabs / Chaw dai khoom hauv lubPua pua milligrams(piv txwv li, 1mg / kg, 3mg / kg, 10mg / kg lossis tsau koob tshuaj zoo li 300mg, 400mg) tswj hwmintravenously lossis subcutaneously, feem ntauTxhua 2-4 lub lis piamCov. Ib qho "1mg" koob tshuaj lom yog cov ntsiab lus tsis muaj qab hau rau kev cuam tshuam rau kev cuam tshuam. Cov koob tshuaj zoo yuav muaj feem ntau thiab kim heev.

Caunch ncig:Hypothetical cyclestej zaumKoom tes nrog cov tshuaj ntau (piv txwv li, txhua lub lim tiam lossis bi {{2} {{{5 lub lis piam, tsom rau kev txhawb nqa kev loj hlob. Lub sijhawm ntxhua khaub ncaws ntxhua yuav ntev ntev vim txuas ib nrab lub neej. Qhov zoo kawg nkaus ntev rau hyperplasia vs. kev pheej hmoo yog tsis paub.

● Ib nrab - lub neej (T1 / 2):Qhov no yog qhov tseem ceeb thiab muaj nce heev:

○ Cov Antibodies Monoclonal:Feem ntau muajntevib nrab - lub neej, feem ntau yog xws li7 txog 21 hnub(xws li, stamulumab ~ 17 hnub). Qhov no ua rau muaj kev txhawb nqa kev txhawb nqa tab sis kuj tseem ua kom raug rau cov kev mob tshwm sim.

○ Soluble recoror decoys:Ib nrab - lub neej muaj peev xwm sib txawv tab sis feem ntau luv dua mabs, muaj feem nyob hauv ntau3-10 hnub(piv txwv li, ace-031 ~ 9 hnub).

○ Peptide / RCS:Yog tias sim ua kom pom tseeb cov no, ib nrab {{{lub neej yuav luv heev (feeb txog kev pheej hmoo siab thiab ua kom muaj kev pheej hmoo ntau ntxiv.

● Post {{0 {}} Kev Kho Mob Siv Tshuaj (PTC) - Qhov kev txhawj xeeb:Tsis zoo li AAS / PEDs qhov twg pct nyob qhov twg ords kom rov ua haujlwm endrosterone, Myostatin Inhibition PTHITE PTHITE PTHEPITY THIAB REV REVOUNDING LUBtom qabntawm hyperplasia thiab peev xwm rov qab.

○ Cov ntaub ntawv txuas ntxiv tsis muaj zog:Lub sijhawmtom qabNres lub inhibitor yuav yog qhov tshwj xeeb tshaj yog - kev pheej hmoo rau cov leeg / Ligament Raug Mob. Tshiab tsim cov leeg leeg cov fibers yuav tsis muaj paub tab, ua ke txhawb nqa cov nqaij mos mos. Kev siv kev kawm yuav tsum tau ceev faj cia - txoj cai.

Muaj peev xwm rov ua haujlwm Atrophy:Yog hais tias kev hloov pauv tau zoo heev, a rov qab nce ntxiv hauv myostatin signalingyuavtheoretically ua rau lub sijhawm ntawm cov leeg ua kom nrawm protein. Cov tswv yim los txo qhov no tsis paub.

Txhawb Nqa Kev Ntsuas:Kev tsom xam yog rau Collagen Synthesis txhawb (vitamin C, Geptin, muaj kev phom sij ntxiv) Muajtsis muajtsim los yog muaj kev nyab xeeb ptc raws tucocol.

Luam Lag Luam	LATENT GDF-8, Myostatin, GDF8, MSTN, Kev Loj Hlob, Txawv Qhov Zoo 8
Cas	271597-12-7
Tus hniav loj	25.6 Kilodalons (KDA)
Cov lus ntawm ib txoj kab ke	375 amino acids
Kev coj dawb huv	Saum toj no 98%
Kev tsim nyog	1mg / vial, lyophilized hmoov

 

 

Kev xav tau, thov hu rau peb

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Lub theoretical muaj peev xwm ntawm myostatin inhibition los account cov leeg tsis tau txais kev loj hlob ntawm hyperplasia yog qhov tsis txaus ntseeg. Txawm li cas los xij, qhov tseeb yog stark. Txoj kev los ntawm kev nkag siab GDF-8 kom muaj kev nyab xeeb, thiab tshwj xeeb ua tsis tau kev phom sij

Cim npe nrov: GDF-8 (Myostatin) 1Mg Rau Cas: 271597-12-7, Tuam Tshoj GDF-8 (Myostatin) 1