Tirzepatid 10mg we yu de yuz

▎ Tirzepatid Strukchɔ

Sos: PubChem

Sikyud: . Tyr-{Aib}-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Tyr-Ser-Ile-{Aib}-Lyu-Asp-Lys-Ile-Ala-Gln-{diasid-C20-gamm a-Glu-(AEEA)2-Lys}-Ala-Fhe-Val-Gln-Trp-Lyu-Ile-Ala-Gly-Gly-Pro-Ser-Ser-Gly-Ala-Pro-Pro-Pro-Ser-NH2 Mɔlikul Fɔmula: C 225H 348N 48O68 Molekyula Weyt: 4813 g/mol CAS Nɔmba: 2023788-19-2 PubChem CID: 163285897, ɛn di ɔda wan dɛn Sinonim dɛn: Zepbound; Mounjaro we de na di wɔl

▎ Tirzepatid Risach

Wetin na di risach bakgrɔn fɔ Tirzepatid?

Tirzepatid na wan sintetik polipεptida drɔg. di risach εn divεlכpmεnt we i de du kכmכt frכm dip כndastandin fכ di limitεshכn dεm fכ di GLP-1 rεsεptכr agonist dεm we de naw fכ trit tayp 2 dayabεtis εn fכ fat da tεm de. pan ɔl we di GLP-1 riseptɔ agonist dɛn dɔn sho fayn fayn wok fɔ kɔntrol di glukɔs na di blɔd ɛn fɔ lɔs di wet, sayɛnsman dɛn dɔn si se dɛn aktiveshɔn fɔ di GIP riseptɔ rili wik, we de stɔp di ɛfifikɛshɔn fɔ di drɔgs to sɔm mak. So, di risach ɛn divɛlɔpmɛnt tim bin dɔn mekɔp dɛn maynd fɔ mek wan nyu mɛrɛsin we go ebul fɔ mek ɔl tu di GIPR ɛn GLP-1R aktiv wan tɛm fɔ mek dɛn ebul fɔ kɔntrol di glukɔs na di blɔd ɛn fɔ mek dɛn ebul fɔ kɔntrol di wet we dɛn gɛt mɔ kɔmprɛhnsiv ɛn ifektiv wan ^[1]..

We dɛn bin de du di risach ɛn divɛlɔpmɛnt prɔses fɔ Tirzepatid, sayɛnsman dɛn bin du bɔku bɔku bɛsik risach ɛn klinik trial dɛn. In di prɛklinik risach stej, dɛn yuz animal ɛkspiriɛns fɔ rili evalyu di famakodaynamik prɔpati dɛn fɔ Tirzepatid. Di rizɔlt dɛn kɔnfyus in pɔtnɛshɛl fɔ kɔntrol di glukɔs na di blɔd ɛn fɔ lɔs di wet, we mek di fawndeshɔn fɔ di klinik trial dɛn we go kam afta dat. Afta dat, Tirzepatid bin enta di klinik trial stej, inklud di faz I, II, ɛn III. Faz I men wan bin evalyu di sef, tolerabiliti, ɛn famakokinɛtik prɔpati dɛm fɔ di drɔg, ɛn di rizɔlt sho gud sef ɛn tolerabiliti. Faz II bin fכs εksplכr di efεktiv εn sef fכ difrεn doz dεm pan pasεnshכn dεm wit tayp 2 dayabεtis, fכs dεtermin di ifektiv doz rεnj. Di ki phase III klinik trial dɛm, lɛk di SURPASS siriɔs stɔdi dɛm, involv bɔku bɔku pasɛnt dɛm wit tayp 2 dayabitis. di risalts sho se Tirzepatid bin sכmtεm bכku pas di GLP-1 rεsεptכr agonist dεm we bin de, lεk Semaglutid, fכ ridyus di blכd glukכs εn wet, we gi strכng pruf fכ di makεt aplikεshכn ^[1]..

Tirzepatid na polipεptida we kכmכp fכ 39 amino asid dεm, εn dεn dכn mכdify in strכkchכ fכ impruv in stεbiliti εn fכmakodaynamiks. in yכnik strכkchכral disayn de mek i ebul fכ intagret di ifekt dεm we tu inkrεtin dεm, GIP εn GLP-1, de gi insay wan mכlikul, we de aktibכt di כmon rεsεpכta dεm we de involv fכ kכntrכl di glukכs na di bכdi tru wan tu mεkanism. spεshal wan, na wan say, i de akt pan di pankrias fכ mek insulin sekreshכn εn inhibit glukagon rilis fכ lכs di glukכs na di bכdi; na di כda say, i de wok pan di sεntri nεv sεstem, i de delay di gεstrik εmpti, i de mek yu satisfay, i de rεdכks fכ it εn it, εn i de ajɔst di wet mεnejmεnt. Dis tu mεkanism de gi Tirzepatid yunik advantej dεm na di tritmεnt fכ tayp 2 dayabεtis εn fat, de gi di sik pipul dεm wan mכr kכmprεhεnsiv tritmεnt opshכn ^[1]..

Wetin na di we aw Tirzepatid de wok?

Tirzepatid de lכs di glukכs na di bכdi tru dεn mכltipכl mεkanism dεm ya:

aktibכshכn fכ GLP-1 rεsεpכta dεm: Tirzepatid de biεn di GLP-1 rεsεpכta dεm pan pankrεas beta sεl dεm, we de miks di akshכn fכ nεchכral GLP-1. GLP-1 na כmon we di intestin de mek we rili imכtant fכ mek di glukכs homכstasis mεnten. i kin mek insulin sεntez, sekreshכn, εn glukכs sεns, εn rεdכks glukכn sekreshכn fכ mek yu satiet εn sכpres apεtit. pan di sik pipul dεm we gεt tayp 2 dayabεtis, if insulin nכ de kכmכt כ we di sεl dεm de rεdכks sεnsitiviti to insulin de mek di blɔd glukכs go כp. Tirzepatid de inkrεs insulin sekreshכn bay we i de aktibכt GLP-1 rεsεpכta dεm, we de impruv bכdi glukכs kכntrכl. di sem tεm, di aktibכshכn fכ di GLP-1 rεsεpכta dεm kin inhεbit bak di rilis fכ glukכn, fכ ridyus di sכs dεm fכ di blכd glukכs εn kכntribyut fכ kכntrכl di glukכs na di bכdi ^[2]..

aktibכshכn fכ GIP rεsεpכta dεm: Tirzepatid de akt pan GIP rεsεpכta dεm, εn in aktibכshכn kin εnhans insulin sεnsitiviti εn sekreshכn. di GIP risεptor dεm de mεntal insay tisu dεm lεk pankrεas beta sεl dεm. afta aktibכt, tru intasεlulyar signal path transdyushכn, insulin sekreshכn de inkrεs, εn di sεl in rεspכns to insulin de εnhans, we de ridyus di blכd glukכs mכr ifektiv wan ^[2] . dis dual risεptor agonist ifekt de mek Tirzepatid mכr ifektiv pas singl GLP-1 rεsεpכta agonist dεm fכ protεkt insulin sekreshכn εn inhεbit glukagon rilis ^[2]..

Dilay fɔ Ɛmpti di Gɛst ɛn fɔ mek pɔsin satisfay: Tirzepatid kin delay fɔ ɛmti di bɛlɛ, i kin mek di it fɔ lɔng tɛm we i de it na di bɛlɛ, i kin mek di rit we di it de tek di it slo, ɛn i kin mek di blɔd glukɔs we de na di blɔd nɔ go ɔp bad bad wan. di ifekt we i gεt pan di gεstrik εmpti de kכmparabl wit di wan we di GLP-1 rεsεpכta agonist dεm de gi. pan di sem tεm, i de akt pan di sεntri nεv sεstem, i de mek yu satisfay, i de rεdכks di apεtit εn di it we yu de it, we fayn fכ di fat prכblεm we bכku tεm kin kam wit di sik pipul dεm we gεt tayp 2 dayabεtis, i de εp fכ impruv insulin rεsistεns εn di כvala mεtabolik kכndishכn ^[2]..

Impruv Insulin Sεnsitiviti εn Lipid Mεtabolism: Tirzepatid kin inkrεs di lεvεl fכ adiponectin, wan adipocytokine we riliyt to insulin sεnsitiviti, we de εp fכ impruv insulin sεnsitiviti, mek di sεl dεm ebul fכ tek εn yuz glukכs mכr ifektiv wan, εn ridyus di glukכs na di bכdi (Anonymous, 2023). apat frכm dat, i kin impruv di lipid profayl bak, we gεt pכtεnshal prכtektiv ifekt pan di kכdivaskyul hεlth. Dɛn dɔn pruv se i ebul fɔ mek blɔd prɛshɔn bɛtɛ, ridyus LDL kɔlɔstrel ɛn triglisɛrɛyd ^[3]..

Sos: PubMed ^{[5] we dɛn pul am.}

Wetin na di stɔdi dɛn we gɛt fɔ du wit dis?

Efficacy pan Weight Management in Patient dɛm wit Ɔbisiti ɛn Tayp 2 Dayabitis

Bɔku klinik stɔdi dɛn dɔn kɔnfyus se Tirzepatid gɛt impɔtant weit lɔs ifɛkt. Insay di 'SURMOUNT-2' stεdi, dεn bin du dis fεz 3, dכbl-blaynd, randomizεd, plasεbo-kכntrol trial na sεvin kכntri dεm. Adult (we ol ≥ 18 ia) wit BMI we na 27 kg/m² ɔ ay pas dat ɛn HbA2c we na 7 - 10% bin inrɔl ɛn randomly asaynd fɔ gɛt wan tɛm ɛvri wik sabkyutan injɛkshɔn fɔ Tirzepatid (10 mg ɔ 15 mg) ɔ plasɛbo fɔ 72 wik. Di risal sho se na wik 72, di pasɛnt we di wet lɔs na di Tirzepatid 10 mg ɛn 15 mg grup na bin -12.8% ɛn -14.7% rispɛktvɔli, kɔmpia wit -3.2% na di plasɛbo grup. Di ɛstimat tritmɛnt difrɛns fɔ Tirzepatid 10 mg ɛn 15 mg kɔmpia wit di plesibo na bin -9.6 pasɛnt poɛnt ɛn -11.6 pasɛnt poɛnt rispɛktvɔli, we bin stɛtistikli sifyukɛnt (p < 0.0001). Apat frɔm dat, mɔ pasɛnt dɛn we bin de gɛt Tirzepatid tritmɛnt bin rich di trɛshɔld fɔ 5% ɔ mɔ wet lɔs (79 - 83% vs 32%) (Garvey WT, 2023). Insay dis stכdi, di avεrej beslayn wet na bin 100.7 kg, di BMI na bin 36.1 kg/m², εn di HbA0 na bin 8.02%. Afta 72 wiks we dɛn trit am, Tirzepatid nɔ bin jɔs ridyus di bɔdi wet bad bad wan bɔt i bin gɛt fayn ifɛkt pan kɔntrol glukɔs na di blɔd ^[4]..

Improvement of Dayabitik Nyuropati

Stɔdi dɔn sho se GLP1-RA kin ridyus di risk fɔ gɛt dis maynia sik pan pipul dɛm wae gɛt tayp 2 dayabitis bay wae dɛn kin mɛmba, lan, ɛn win di kɔgnitiv impairment. as dual GIP-RA/GLP-1RA, insay di nyuroblastoma sel layn (SHSY5Y), risεch dεn fכnshכn se Tirzepatid gεt impak pan mak dεm fכ nyuronal growth (CREB εn BDNF), apoptosis (BAX/Bcl2 rεshכ), difrεns (pAkt, MAP2, GAP43, εn AGBL4), εn insulin rεsistεns (GLUT1, GLUT4, GLUT3, εn SORBS1). di rizulεt dεm εnfaz di rol we Tirzepatid de ple fכ aktibכt di pAkt/CREB/BDNF path εn dכwnstrim signal kaskad dεm εn in nyuroprotεktiv efikכs, we sho se i kin kכntrכl di ifekt dεm we de asai wit haypa glycemia εn insulin rεsistεns na di nyuronal lεvεl. fכ dat, Tirzepatid kin impruv di nyurodijεnεreshכn we de kכz fכ haypa glycemia εn i kin כvakom nyuronal insulin rεsistεns, we de gi nyu insayt fכ di impruvmεnt fכ di nyuropathy we de rilet to dayabitis ^[5]..

Risach Prɔgrɛs pan di Tritmɛnt fɔ Tayp 2 Dayabitis

As nyu kayn haypoglycemic drɔg, Tirzepatid dɔn bi di fɔs dual GIP/GLP-1R agonist we dɛn dɔn gri fɔ trit dayabitis na Amɛrika. Bɔku big big klinik trial dɛn dɔn kɔnfyus se i de mek di glukɔs we de na di blɔd go dɔŋ ɛn i de mek i nɔ gɛt bɔku bɔku bɔdi, ɛn i gɛt di pawa fɔ protɛkt di at ɛn di blɔd. di kכnsεpt fכ sεntetik pεptida dεn dכn opin plεnti posisibul dεm we dεn nכ no fכ Tirzepatid. di trayal dεm we de go bifo (NCT04166773) εn pruf dεn sho se na prכmis drog insay di fil dεm fכ nכn-alkohol fεt liva sik (NAFLD), rεnal εn nyuroprotεkshכn ^[6] (Ma Z, 2023).

Lכng tεm Impekt כf Tirzepatid pan Kadivaskyul Hεlth

Tirzepatid kin ridyus di risk fɔ gɛt sik dɛn we de ambɔg di at ɛn di blɔd bay we i de mek pɔsin lɔs in wet. Wan stכdi bin egzamin di impak we Tirzepatid gεt pan di fat εn di kכdivaskyul sik ivent dεm pan di big pipul dεm na Amɛrika ^[7] . Di stכdi fכnshכn se pan Amεriכn big pipul dεm we fit fכ Tirzepatid tritmεnt, afta tritmεnt wit 15 mg Tirzepatid, dεn εstimat 70.6% εn 56.7% pan di big pipul dεm lכs ≥ 15% εn ≥ 20% pan dεn bכdi wet rispεktivli, we min se 58.8% ridyus pan di nכmba כf pipul dεm we fat. Na di wan dɛm we nɔ gɛt kadyovaskular sik, di ɛstimat 10 ia kadiovaskular sik risk dɔn go dɔŋ frɔm 10.1% 'bifo tritmɛnt' to 7.7% 'afta tritmɛnt', wit absɔlɔb risk ridɔkshɔn fɔ 2.4% ɛn rilitiv risk ridɔkshɔn fɔ 23.6%, we mek 2 milyɔn kadiovaskular sik ivin dɛm nɔ apin.

fכ kכnklud, Tirzepatid na nyu tכp dual agonist fכ GIP εn GLP-1 rεsεpכta dεm, we gεt big minin fכ di tritmεnt fכ tayp 2 dayabεtis εn fכ fat. I kin mek insulin sekreshɔn fayn fayn wan, stɔp glukagon sekreshɔn, rigul di glukɔs na di blɔd prɛsishɔn, ridyus di risk fɔ kɔmplikeshɔn, impruv di wok we pankrias beta sɛl dɛn de du, delay di prɔgrɛs fɔ dayabitis, ɛn i gɛt ɛfɛkt fɔ protɛkt di at. We dɛn de trit pipul dɛn we fat, i kin rili ridyus di it we dɛn de it, nɔ want fɔ it, i kin mek dɛn satis, ɛp di wan dɛn we fat fɔ lɛ dɛn nɔ gɛt bɔku bɔku bɔdi, ɛn i kin mek dɛn nɔ gɛt prɔblɛm dɛn we kin apin we dɛn fat pasmak. I kin mek bak di insulin rɛsistɛns ɛn lipid mɛtabolism bɛtɛ. Apat frɔm dat, i de sho se i kin ebul fɔ trit sik dɛn we gɛt fɔ du wit mɛtabolik abnɔmal tin lɛk stiatohepatitis we nɔ de drink rɔm, slip apnia sindrom, ɛn at pwɛl, ɛn i kin mek bɔku mɛtabolik indikɛtɔ dɛn bɛtɛ wan tɛm, we kin gi mɔ kɔmprɛhnsiv tritmɛnt plan. Di we aw dɛn kin injɛkshɔn wan tɛm insay di wik kin izi fɔ yuz ɛn i kin mek di sikman dɛn fala di tritmɛnt fayn fayn wan. We i kɔntrol di glukɔs ɛn wet na di blɔd fayn fayn wan ɛn ridyus di risk fɔ gɛt prɔblɛm dɛn, i kin rili ɛp fɔ mek di sikman dɛn bɔdi bɛtɛ, i kin mek dɛn ebul fɔ du tin dɛn ɛvride ɛn kwaliti layf, i kin mek dɛn gɛt kɔnfidɛns fɔ kɔntrol di sik, i kin mek dɛn nɔ gɛt bɔku prɔblɛm wit dɛn maynd, ɛn i kin mek dɛn ebul fɔ adap to ɔda pipul dɛn.

Bɔt di pɔsin we rayt di buk

Di tin dɛm we wi dɔn tɔk bɔt ɔp na ɔl di risach, ɛdit ɛn kɔmpilayt na Cocer Peptidd glukכs. Apat frɔm dat, dɛn dɔn fulɔp fɔ chɛk di kadyovaskyuɛl prɔtɛktiv ifɛkt fɔ dis drɔg, we kin ridyus di risk fɔ big bad bad tin dɛn we kin apin to di at ɛn di blɔd bay 26%, we kin gi ɔda tritmɛnt bɛnifit fɔ di wan dɛn we gɛt dayabitis we gɛt sik dɛn we de ambɔg di at ɛn di blɔd. Apat frɔm di tritmɛnt fɔ dayabitis, dɛn kin yuz semaglutide fɔ di lɔng tɛm mɛnejɛmɛnt fɔ fat ɛn i dɔn sho se i kin gɛt pɔtnɛshɛl tritmɛnt valyu pan klinik risach pan sik dɛm lɛk nɔ-alkohol stiatohepatitis ɛn Alzaima sik.

Sayɛns Jɔnal Author

Dɔktɔ Wiliam T. Gavi na wan big masta sabi bukman ɛn risachman we gɛt fɔ du wit bɔku bɔku big big institiushɔn dɛn, lɛk di Yunivasiti ɔf Alabama na Bɛmingham, Aston Yunivasiti, ɛn di Bɛmingham Veterans Afɛj Mɛdikal Sɛnta. In akademik bakgrɔn ɛn in wok ɛkspiriɛns span bɔku difrɛn disiplin dɛn insay di mɛdikal ɛn sayɛns fild dɛn. Dɔktɔ Garvey dɔn mek bɔku kɔntribyushɔn to di fild dɛm fɔ ɛndokrinɔlɔji ɛn mɛtabolism, nyutrishɔn ɛn itɛttiks, bayɔkemistri ɛn mɔlikul bayoloji, ɛn bak jenɛral ɛn intanɛnt mɛrɛsin, wit patikyula fɔs pan di kadiovaskular sistɛm ɛn kadiɔlɔji. Bɔku pipul dɛn dɔn no ɛn ɔnɔ in wok, mɔ we dɛn kɔl am Highly Cited Researcher in di Cross-Field kategori fɔ ɔl tu di 2023 ɛn 2024, we sho di big impak ɛn inflɛns we in risach gɛt pan di brayt sayɛns kɔmyuniti.

Dכkta Garvey in risach intres εn εkspεriεns de εksεnd to difrεn aspek dεm fכ mεtabolik sik dεm εn dεn mεnejmεnt. I dɔn de wok tranga wan fɔ stɔdi bɔt dayabitis, fɔ fat, ɛn di prɔblɛm dɛn we gɛt fɔ du wit dɛn, ɛn i dɔn aim fɔ fɛn nyu tritmɛnt strateji ɛn fɔ mek di pɔsin gɛt bɛtɛ tin fɔ du. In wok inkɔmpas besik sayɛns risach, klinik trial, ɛn transleshɔnal stɔdi, we de briŋ di gap bitwin di tin dɛn we dɛn dɔn fɛn na lɛbɔretri ɛn di rial wɔl mɛdikal aplikeshɔn dɛn. Tru in bɔku risach, Dɔkta Garvey dɔn kɔntribyut fɔ ɔndastand mɔ bɔt di ɔndalayn mɛkanism dɛm fɔ mɛtabolik dizayd ɛn i dɔn ɛp fɔ shep klinik gaydlayn ɛn tritmɛnt protɔkɔl dɛm na di fild fɔ ɛndokrinɔlɔji ɛn mɛtabolism. Dɛn rayt Dɔktɔ Wiliam T. Gavi insay di rɛfrɛns fɔ saytayshɔn ^[4 ].

▎ Saytayshɔn dɛn we gɛt fɔ du wit dis

[1] Nowak M, Nowak W, Grzeszczak W. Tirzepatid - wan dual GIP/GLP-1 rεsεptכr agonist - wan nyu antidiabetic drog wit pכtεnshal mεtabolik aktiviti in di tritmεnt fכ tayp 2 dayabεtis[J]. Ɛndokrinɔlɔjia Polska, 2022,73(4):745-755.DOI:10.5603/EP.a2022.0029.

[2] Nɔbɔdi nɔ no in nem. Tirzepatid: Na Dual Glucose-Dipεndεnt Insulinotropik Polipεptida εn Glucagon-Lεk Pεptid-1 Agonist fכ di Mεnejmεnt fכ Tayp 2 Dayabitis Mεlitus: Erratum.[J]. Amɛrikan Jɔnal fɔ Tɛrapi, 2023,30(3):e311.DOI:10.1097/MJT.0000000000001634.

[3] Fɔrzano I, Varzideh F, Avvisato R, ɛn ɔda pipul dɛn. Tirzepatid: Wan Sistɛm Ɔpdet[J]. Int ɛ rnash ɔ nal J ɔ rnal ɔ f Mɔlikul Sayns, 2022,23(23).DOI:10.3390/ijms232314631.

[4] Garvey WT, Frias JP, Jastreboff A. M., ɛn ɔda pipul dɛn. Tirzepatid wan tɛm ɛvri wik fɔ di tritmɛnt fɔ fat pan pipul dɛn we gɛt tayp 2 dayabitis (SURMOUNT-2): na dabl-blaynd, randomised, multicentre, placebo-controlled, phase 3 trial[J]. Lancet, 2023,402(10402):613-626.DOI:10.1016/S0140-6736(23)01200-X.

[5] Fontanella R. A., Ghosh P., Pɛsapane A, ɛn ɔda pipul dɛn. Tirzepatid de mek nyurodijεnεreshכn tru mכltipכl mכlikul path dεm[J]. J ɔ rnal ov Transleshɔnal Mɛdisin, 2024,22(1).DOI:10.1186/s12967-024-04927-z.

[6] Ma Z, Jin K, Yue M, ɛn ɔda pipul dɛn. Risach Prɔgrɛs pan di GIP/GLP-1 Risɛptɔ Kɔagonist Tirzepatid, wan Rising Sta insay Tayp 2 Dayabitis[J]. J ɔ rnal ɔ f Dayabitis Risach, 2023,2023.DOI: 10.1155/2023/5891532.

[7] Wong ND, Karthikeyan H, Fan W. US Populεshכn Eligibiliti εn εstimatεd Impεkt כf Tirzepatid Tritmεnt pan Obesity Prεvalεns εn Kadivaskyul Disiz Ivent dεm[J]. Kardiovaskular Drug ɛn Tɛrapi, 2024.DOI: 10.1007/s10557-024-07583-z.

ƆL DI ATIKUL ƐN PRODƆKT INFƆMƐSHƆN WE DƐN GI NA DIS WƐBSAYT NA FƆ ƆL DI INFƆMƐSHƆN DISƐMƐNƐSHƆN ƐN FƆ EDYUKESHƆN.  

Di prɔdak dɛn we dɛn gi na dis wɛbsayt na fɔ in vitro risach nɔmɔ. in vitro risach (Latin: *in glas*, we min insay glas) dεn de du am ausayd mכtalman bכdi. Dɛn prɔdak ya nɔto mɛrɛsin, dɛn nɔ gɛt di aprɔval frɔm di US Food and Drug Administration (FDA), ɛn dɛn nɔ fɔ yuz dɛn fɔ protɛkt, trit, ɔ mɛn ɛni mɛrɛsin, sik, ɔ sik. Di lɔ nɔ gri fɔ mek dɛn put dɛn tin ya insay mɔtalman ɔ animal bɔdi ɛni we.