GLP-2 90mg

▎ GLP-2 Struktrɔ

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-Phe-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

▎ GLP-2 Risach

Wetin na di risach bakgrɔn fɔ GLP-2?

GLP-2 na sεntetik polipεptida dכg, εn in divεlכpmεnt kכmכt frכm dip כndastandin fכ di limitεshכn dεm fכ di GLP-1 rεsεptכr agonist dεm we de naw insay di tritmεnt fכ tayp 2 mεtabolism mεlitus εn fכ fat. pan ɔl we di GLP-1 rεsεptכr agonist dεn dכn sho se dεn de du fayn fayn wan fכ kכntrכl di blכd glukכs εn fכ lכs di wet, sayɛnsman dεm dכn fכnshכn se pan כl we dεn de aktibכt di GLP-1 rεsεptכr, dεn aktibכshכn ifekt pan di GIP rεsεptכr wik, we to wan sכm mak de limited di tεrapi ifekt fכ di dכg dεm. So, di risach ɛn divɛlɔpmɛnt tim dɔn mekɔp dɛn maynd fɔ mek wan nyu kayn drɔg we go ebul fɔ mek ɔl tu di GIPR ɛn GLP-1R aktiv wan tɛm, wit di op 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 fayn fayn wan ^[1]. .

Insay di risach ɛn divɛlɔpmɛnt prɔses fɔ GLP-2, sayɛnsman dɛn dɔn du bɔku bɔku bɛsik risach ɛn klinik trayal dɛn. Fɔs, insay di prɛklinik risach stej, dɛn bin dip dip wan fɔ evaluate di famakodaynamik kwaliti dɛn fɔ GLP-2 tru animal ɛkspiriɛns, ɛn dɛn bin verify in pɔtnɛshɛl fɔ kɔntrol di glukɔs na di blɔd ɛn fɔ lɔs di wet. di risal sho se GLP-2 kin ridyus di blכd glukכs lεvεl bכku bכku wan na animal mכdel dεm εn i kin du fayn bak pan wet mεnejmεnt. Dɛn fayn fayn tin ya we dɛn fɛn bin mek wan strɔng fawndeshɔn fɔ di klinik trayal dɛn we dɛn bin du afta dat.

Afta dat, GLP-2 enta di klinik trial stej, inklud faz I, II, ɛn III trayal. Insay di faz I trayal, dɛn bin men wan fɔ ɛvaluet di sef, tolɛrabiliti, ɛn famakokinɛtik kwaliti dɛn fɔ di drɔg, ɛn di rizɔlt dɛn sho se GLP-2 bin gɛt gud sef ɛn tolɛrabiliti. Di fεz II trayal fכs εksplכr di efεktiv εn sef fכ difrεn dכz dεm fכ GLP-2 in pasεnshכn dεm wit tayp 2 mεtabolism mεlitus, εn fכs dεtermin in ifektiv dכz rεnj. Di mכst krεs fכs III klinik trial dεm, lεk di SURPASS siriכs stכdi dεm, kכba wan big nכmba כf pasεnshכn wit tayp 2 mεtabolism mεllitus. di risalts sho se GLP-2 bin sכmtεm sכpεriכr pas di GLP-1 rεsεptכr agonist dεm we bin de, lεk GLP-1, fכ ridyus di blכd glukכs εn wet. Dis brekthru risal giv strכng pruf sכpכt fכ di makεt aplikεshכn fכ GLP-2 ^[1]..

GLP-2 na polipεptida we kכmכp fכ 39 amino asid dεm, we dεn dכn mכdify wan wan amino asid dεm strכkchכral fכ impruv in stεbiliti εn efficacy. dis yכnik strכkchכral disayn de mek GLP-2 ebul fכ intagret di ifekt dεm fכ tu inkrεtin כmon dεm, GIP εn GLP-1, insay wan mכlikul, εn aktibכt di כmon rεsεpכta dεm we de involv fכ kכntrכl di glukכs na di bכdi tru wan tu mεkanism fכ akshכn. spεshal wan, GLP-2 kin akt pan כl tu di pankrias εn di sεntri nεv sεstem. na wan say, i de mek insulin sekreshכn εn i de mek di glukagon kכmכt, we de mek di glukכs we de na di bכdi dכn fayn fayn wan; na di כda say, bay we i de delay fכ ɛmti di gεstrik εn i de mek i satisfay, i de ridyus di fכ it εn di it we i de it, εn dis de mek i ebul fכ mεnεj di wet. dis tu mεkanism fכ akshכn de gi GLP-2 yunik advantej dεm fכ trit di tayp 2 mεtabolism mεllitus εn fכ fat, we de gi di sik pipul dεm wan mכr kכmprεhεnsiv tritmεnt opshכn ^[1]..

Wetin na di mεkanism fכ akshכn fכ GLP-2?

GLP-2 de lכs di glukכs na di bכdi tru mכltipכl mεkanism dεm we de wok tכgeda, lεk dis: Aktibכshכn fכ di GLP-1 rεsεpכta: GLP-2 de biεn di GLP-1 rεsεpכta pan pankrεas β sεl dεm, we de miks di ifekt we nεchכral GLP-1 de gi. GLP-1 na כmon we dεn prodyuz na di intestin εn i implεnt fכ mεnten glukכs homכstasis 2. I kin mek insulin sεntesis, insulin sekreshכn, εn glukכs sεns, εn ridyus glukכn sekreshכn fכ mek yu satiet εn inhibit apetit 2.

dis aktibכshכn kin mek insulin sekreshכn. insulin na di men ɔmon we de mek di blɔd glukɔs go dɔŋ na di bɔdi, we kin mek di sɛl dɛn tek di glukɔs ɛn yuz am mɔ ɛn mɔ, ɛn dis kin mek di glukɔs we de na di blɔd go dɔŋ. pan di sik pipul dεm we gεt tayp 2 mεtabolism mεlitus, insulin sekreshכn nכ de infεkt כ di sεl dεm in sεnsitiviti to insulin de rεdכks, we de mek di blכd glukכs inkrεs. GLP-2 de inkrεs insulin sekreshכn bay we i de aktibכt di GLP-1 rεsεpכta, we de εp fכ impruv di bכdi glukכs kכntrכl. di sem tεm, di aktibכshכn fכ di GLP-1 rεsεpכta kin inhεbit di rilis fכ glukagon bak. di glukogכn kin mek di glycogenolysis εn gluconeogenesis insay di fast stet, we de mek di bכdi glukכs prodakshכn go כp. bay we i de inhεbit di ifekt we glukכn de gi, GLP-2 de ridyus di sכs fכ di blכd glukכs mכr, we de εp fכ kכntrכl di blכd glukכs ^[2] (Anonymous, 2023).

aktibכshכn fכ di GIP rεsεpכta: GLP-2 de akt pan di GIP rεsεpכta di sem tεm. afta i aktibכt, i kin εnhans insulin sεnsitiviti εn sekreshכn. di GIP risεptor de mεntal insay tisu dεm lεk pankrεas β sεl dεm. afta aktibכshכn, tru di kכndukshכn fכ di intasεlulyar signal path, insulin sekreshכn de inkrεs, εn di sεl dεm in rεspכns to insulin de impruv, we de mek i de ridyus di blכd glukכs 2 mכr ifektiv wan mεtabolism mεlitכs as adjunkt to it εn εksεsayz 2. GLP-2 na sεntetik kεmikכl strכkchכ we de bays pan di GIP sikεns, we kכmכp fכ 39-amino asid pεptida. i de mek insulin sekreshכn bכku, i de ridyus di rilis fכ glukכn we dipεnd pan glukכs, i de lכs di fast εn afta it bכdi glukכs lεvεl, i de mek yu satis, i de ridyus di wet, εn i de delay di gεstrik εmpti 2.

dis dual risεptor agonist ifekt de mek GLP-2 mכr ifektiv fכ protεkt insulin sekreshכn εn inhibit glukagon rilis pas singl GLP-1 rεsεpכta agonist dεm ^[2]..

dilay di gastric εmpty εn inkrεs satiety: GLP-2 kin delay gastric εmpty, lכng di rεsidεns tεm fכ it na di bεlε, slo dכn di absכpshכn rεt fכ di nyutriεnt dεm, εn so i kin avכyd shap inkrεs pan postprandial bכdi glukכs. insay prεklinik εn klinik stכdi dεm, di ifekt we GLP-2 gεt pan gεstrik εmpti de kכmparabl wit di wan we GLP-1 rεsεptכr agonist dεm gεt. insay di it-induced obese mice, di digri fכ dilay gastric εmpty by GLP-2 na di sem lεk di wan fכ GLP-1, bכt dεn akyu inhibitory ifekt dεm ya de disappear afta 2 wiks fכ tritmεnt. insay patisipan dεm wit εn witout tayp 2 mεtabolism mεlitus, wan tεm insay wik GLP-2 (≥5 εn ≥4.5mg, rispεktivli) delay gastric εmpti afta wan singl dכz. In hεlty patisipan dεm, dis ifekt bin atεnuet afta mכltipכl dכz כf GLP-2 כ dulaglutide ^[3]. .

pan di sem tεm, i kin akt bak pan di sεntri nεv sεstem, i kin mek i satisfay, εn i kin mek i nכ want fכ it εn i nכ de it. bay we i de kכntro di it we dεn de it, i de εp indaykt wan fכ kכntrכl di blכd glukכs lεvεl, spεshal wan we fit fכ di fat prכblεm we bכku tεm de wit di sik pipul dεm we gεt tayp 2 mεtabolism mεlitus, εn i de εp fכ impruv insulin rεsistεns εn di כvala mεtabolik stetכs ^[2]..

fכ impruv insulin sεnsitiviti εn lipid mεtabolism: dεn fכnshכn se GLP-2 de inkrεs di lεvεl fכ adiponectin, we na adipocytokine we riliyt to insulin sεnsitiviti. we di lεvεl fכ adiponectin inkrεs de εp fכ impruv insulin sεnsitiviti, mek di sεl dεm mכr sεnsitiv to insulin, εn dis de mek dεn tek εn yuz glukכs fayn fayn wan, we de ridyus di glukכs na di bכdi ^[2]..

apat frכm dat, GLP-2 kin impruv di lipid profayl bak εn i gεt pכtεnshal prכtektiv ifekt pan di kכdivaskyul hεlth. dεn pruv se GLP-2 ebul fכ impruv bכdi prεshכn, rεdכks lכw dεnsiti lipoprotein (LDL) kכlestכl εn triglisεrayd ^[4] .Dis de sכpכt in kכmprεhεnsiv bεnεfit dεm fכ mεnejmεnt di blכd glukכs.

Risach we gɛt fɔ du wit dis

Efikכs pan wεt mεnejmεnt in pasεnshכn dεm we fat εn tayp 2 mεtabolism mεllitus: 

Bɔku klinik stɔdi dɛn dɔn kɔnfyus signifyant weit lɔs ifɛkt: Insay wan stɔdi we dɛn kɔl 'SURMOUNT-2', dis trayal na bin wan faz 3, dɛbul-blaynd, randomiz, plasɛbo-kɔntrol trial we dɛn bin du na sɛvin kɔntri dɛn. Adult (we ol ≥18 ia) wit bɔdi mas indeks (BMI) we na 27 kg/m² ɔ i pas dat ɛn wan glycated hemoglobin (HbA1c) we na 7 - 10% dɛn bin randomly asaynd fɔ gɛt wan tɛm insay di wik sabkyutan injɛkshɔn fɔ GLP-2 (10mg ɔ 15mg) ɔ plasɛbo fɔ 72 wik. Di risal sho se na wik 72, di pasɛnt we di wet lɔs na di GLP-2 10mg ɛn 15mg grup na bin -12.8% ɛn -14.7%, rispɛktvɔli, we di wan na di plasɛbo grup na -3.2%. Di ɛstimat tritmɛnt difrɛns fɔ GLP-2 10mg ɛn 15mg kɔmpia wit di plesibo na bin -9.6 pasɛnt poɛnt ɛn -11.6 pasɛnt poɛnt, rispɛktvɔli, dɛn ɔl tu na bin statystikal sifyukɛnt (p 0.0001). apat frכm dat, mכr pasεnshכn dεm we dεn trit wit GLP-2 rich di thrεshold fכ weit lכs 5% כ mכr (79 - 83% vs 32%) ^[5] (Garvey WT, 2023). I n di 'SURMOUNT-2' st ɔ di, di beslayn avrej wet na bin 100.7 kg, di BMI na bin 36.1 kg/m², ɛn di HbA1 na bin 8.02%. afta 72 wiks we dεn trit am, GLP-2 nכto nכmכ rεdכks di wet bכku bכt i bin ple fayn rol fכ kכntrכl di glukכs na di b ^{כdi [5].}.

Improvεmεnt ifekt pan mεtabolism-rεlatεd nyuropathy: 

Sɔm stɔdi dɔn sho se glukagon-layk peptide 1 rεsεptכr agonist dεm (GLP1-RA) kin ridyus di risk fכ dimεnshכn pan pasεn dεm we gεt tayp 2 mεtabolism mεlitus bay we dεn de impruv mεmכri, lan, εn כvakom di kכgnitiv impεryans. as dual glukoz-dipεndεnt insulin polypεptida rεsεptכr agonist (GIP-RA)/GLP-1RA, dεn stכdi GLP-2 fכ in ifekt dεm 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) in wan nyuroblastoma sel layn (SHSY5Y). di rizulεt fכ di fכs tεm εnfaz di rol we GLP-2 de ple fכ aktibכt di pAkt/CREB/BDNF path εn dכwnstrim signal kaskad, εn bak in efikכs in nyuroprotεkshכn. i sho bak se GLP-2 kin kכntrכl di ifekt dεm we riliyt to haypa glycemia εn insulin rεsistεns na di nyuronal lεvεl. fכ dat, GLP-2 kin impruv di nyurodijεnεreshכn we kכz bay haypa glycemia εn i kin כvakom nyuronal insulin rεsistεns, we de gi nyu insayt fכ di impruvmεnt fכ di mεtabolism-rεlatεd nyuropathy ^[6]. .

Risach prɔgrɛs pan di tritmɛnt fɔ tayp 2 mɛtabolism mɛlitɔs: 

Sɔm stɔdi dɛn dɔn sho se GLP-2, as nyu kayn haypoglycemic drɔg, dɔn bi di fɔs dual GIP/GLP-1R agonist we dɛn dɔn apruv fɔ trit mɛtabolism na Amɛrika. Dɛn dɔn kɔnfyus se i gɛt impɔtant blɔd glukɔs-lɔr ɛn weit lɔs ifɛkt pan bɔku big-big klinik trial dɛm, ɛn pruf de fɔ se i gɛt bɔku pɔtnɛshɛl bak fɔ protɛkt di at ɛn di blɔd. apat frכm dat, di kכnsεpt fכ sεntetik pεptida dεn dכn opin plεnti posisibul dεm we dεn nכ no fכ GLP-2. di trayal dεm we de go bifo (NCT04166773) εn pruf dεn sho se i tan lεk se na prכmis drog na di fil dεm fכ nכn-alkohol fεt liva sik (NAFLD), rεnal εn nyuroprotεkshכn, εtk ^[7]..

Lɔng tɛm ifɛkt dɛm we T irzepatide gɛt pan di kadiovaskular wɛlbɔdi: 

GLP-2 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 GLP-2 gεt pan di fat εn di kכdivaskyul sik ivent dεm pan Amɛrikan big pipul dεm ^[8] . Di stכdi fכnshכn se pan Amεriכn big pipul dεm we fit fכ GLP-2 tritmεnt, afta tritmεnt wit 15mg GLP-2, dεn εstimat se 70.6% εn 56.7% pan di big pipul dεm bin gεt weit lכs ≥15% εn ≥20%, rispεktivli, we min se di nכmba כf pipul dεm we fat i dכn dכn bay 58.8%. Na pipul dɛm wae nɔr gɛt dis sik na dɛn at, di ɛstimat 10 ia risk fɔ gɛt di sik dɛm wae de kam pan di at ɛn di blɔd kin go dɔŋ frɔm 10.1% bifo tritmɛnt to 7.7% afta tritmɛnt, we sho se di risk ridyus na 2.4% ɛn di risk ridyus na 23.6%, we min se dɛn kin ebul fɔ protɛkt 2 milyɔn sik wae kin apin insay 10 ia.

fכ kכnklud, GLP-2 na nכvel dual agonist fכ GIP εn GLP-1 rεsεpכta dεm εn i gεt big signifyans fכ di tritmεnt fכ tayp 2 mεtabolism mεlitus εn fכ fat. i kin mכr ifektiv fכ mek insulin sekreshכn, inhibit glukagon sekreshכn, prεsisli rεgεl di bכdi glukכs, rεdכks di risk fכ komplikεshכn, impruv di fכnshכn fכ pankrεas β sεl dεm, εn delay di prכgreshכn fכ mεtabolism. I gɛt ɛfɛkt bak we de protɛkt di at ɛn di blɔd sistɛm. We dɛn de trit pipul dɛn we fat, i kin rili ridyus di it we dɛn de it, mek dɛn nɔ want fɔ it, i kin mek dɛn satis, ɛp di wan dɛn we fat fɔ lɛf fɔ it bɔku bɔku it dɛn, 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 abnɔmaliti 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 gi injɛkshɔn wan tɛm insay di wik kin izi fɔ yuz ɛn i kin mek di sikman dɛn fala di tritmɛnt we dɛn de gi dɛn. We dɛn kɔntrol di glukɔs ɛn wet na di blɔd fayn fayn wan ɛn ridyus di risk fɔ gɛt prɔblɛm dɛn, dɛn kin mek di sikman dɛn bɔdi fayn bad bad wan, dɛn kin ebul fɔ du tin dɛn ɛvride ɛn dɛn kin gɛt mɔ kwaliti fɔ liv, dɛn kin gɛt mɔ kɔnfidɛns fɔ kɔntrol di sik, dɛn kin pul dɛn maynd prɔblɛm, ɛn dɛn kin ebul fɔ adap to ɔda pipul dɛn.

Bɔt di pɔsin we rayt di buk

Di tin dɛm we wi dɔn tɔk bɔt, na ɔl di tin dɛm we Cocer Peptides dɔn du risach, ɛdit ɛn kɔmpilayt.

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 fil 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 go to difrεn aspek dεm fכ mεtabolik sik dεm εn dεn mεnejmεnt. I dɔn de wok tranga wan fɔ stɔdi di mɛtabolism mɛlit, fɔ fat, ɛn di kɔmplikeshɔn dɛn we gɛt fɔ du wit dɛn, we i aim fɔ fɛn nyu tritmɛnt strateji ɛn fɔ mek di pɔsin in autkam bɛtɛ. 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 disɔda 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 ^[5]..

▎ Saytayshɔn dɛn we gɛt fɔ du wit dis

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

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

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ƆL DI ATIKUL ƐN PRODƆKT INFƆMƐSHƆN WE DƐN GI NA DIS WƐBSAYT NA FƆ ƆL FƆ DI INFƆMƐSHƆN 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 famasitik, 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.