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▎ Wetin na Kagrilintayd?
Cagrilintide na Dual Amylin-Calcitonin Receptor Agonist (DACRA) we dεn disayn bays pan di strכkchכral fכm fכ di amylin mכlikul. bay we i de tכk tכk εn aktibכt di amylin rεsεpכta εn di kalsitonin rεsεpכta wan tεm, i de sho di pכtεnshal fכ mכlti-dimεnshכnal rεguleshכn fכ mεtabolik paramita dεm, inklud mεkanism dεm fכ akshכn lεk weit mεnejmεnt, mεntenεns fכ bכdi glukכs homכstasis, εn apεtit rεguleshכn. di kכnsεpt fכ in risεch εn divεlכpmεnt kכmכt frכm wan dip analisis fכ di fysiolojikal fכnshכn dεm fכ nεchכral amylin: as כmon we pankrεas β sεl dεm de sekret, nεchכral amylin de tek pat pan di rεgulεshכn fכ di blכd glukכs mεtabolism na mכltipכl lεvεl dεm, lεk fכ rεgεl di satiety, inhibit glukagon sekreshכn, εn delay di gastric εmpti. כltu, in klinik aplikεshכn de limited bay sכt haf-layf (lεk 20 minit), we nid fכ gi am fכs tεm.
di kagrilintayd de εksεnd di haf layf to 7 to 8 dez tru mכlikul modifyushכn, so dat de ridyus di frεkuεns fכ administreshכn bכku bכku wan εn i de impruv klinik kכmplians bכku bכku wan. dis lכng-akt disayn nכ de כnli optimiz di kכnvεns fכ dכg dεlivεri bכt i de achy lכng tεm intavεnshכn in mεtabolik dizכrd bay we i de kכntinyu fכ aktibכt di amylin εn kalsitonin rεsεpכta dεm. sכm spεshal wan, Cagrilintide de kכlכbכt kכntribyut fכ di mεntenans fכ di blכd glukכs homכstasis bay we i de inhεbit di pכstprandial glukagon sekreshכn, delay di gεstrik εmpti, εn εnhans di satiety. di sem tεm, in aktibכshכn fכ di kalsitonin rεsεpכta de εnhans di fכnshכn dεm fכ di bon dεnsiti protεkshכn εn apεtit rεgulεshכn mכr. dis mכlti-targεt sinagεstik mεkanism de εndow am wit brayt aplikεshכn prכspεkt dεm fכ tritmεnt fכ fat, tayp 2 mεtabolism mεlitus εn in kכmplikεshכn dεm, εn de gi wan nyu tritmεnt stratεji fכ di kכmprεhεnsiv mεnejmεnt fכ mεtabolik sεndrכm.
▎ Wetin na Semaglutid?
Semaglutid, as lכng-aktin glukagon lεk pεptida-1 (GLP-1) rεsεptכr agonist, dεn dכn yuz am bכku bכku wan insay di klinik tritmεnt fכ tayp 2 mεtabolism mεlitus. bay we i de miks di fisiolכjik fכnshכn dεm fכ nεchכral GLP-1, dis dכg de trigεr mכltipכl mεtabolik rεguleshכn mεkanism dεm afta i aktibכt di GLP-1 rεsεpכta, inklud di εnhansmεnt fכ glukכs-dipεndεnt insulin sekreshכn, di inhibitory rεguleshכn fכ glukכn rilis, di dilay fכ gastric εmpti rεt, εn di sεntri apεtit sכpreshכn ifekt, we de achy di sinagεstik ifekt fכ prεsis kכntrכl fכ blכd glukכs di lεvεl dεm εn di wet mεnejmεnt. I yunik famakokinɛtik prɔpati dɛn de gi am af-layf we go rich 7 dez, we de sɔpɔt wan tɛm insay di wik sabkyutan injɛkshɔn rijim ɔ wan de ɔral administreshɔn mɔd, we de rili ɔptimayz di tritmɛnt ɛkspiriɛns fɔ di pasɛnt dɛn ɛn impruv di mɛrɛsin we dɛn de fala.
di klinik trial data sho se semaglutide kin ridyus di lεvεl fכ glycated hemoglobin (HbA1c) bכku bכku wan bay 1.8%, εn di insidεns fכ haypoglycemic ivent dεm rili lכw, we de gi am wan yכnik advantej fכ mεnejmεnt fכ blכd glukכs. Apat frɔm dat, dɛn dɔn fulɔp fɔ chɛk di kayn we aw dis drɔg de protɛkt di at ɛn di blɔd, 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 mɛtabolism, dɛn kin yuz sɛmaglutayd fɔ di lɔng tɛm mɛnejɛmɛnt fɔ fat ɛn i dɔn sho se i kin gɛt pɔtɛnɛshɛl tritmɛnt valyu na klinik risach pan sik dɛm lɛk nɔ-alkohol stiatohepatitis ɛn Alzaima sik.
dis mכlti-target tritmεnt mεkanism we bεys pan GLP-1 rεsεptכr aktibכshכn nכto כnli kכmprεhεnsiv כptimayz mεtabolik paramita dεm bay we i de impruv insulin sεnsitiviti, inhεbit pasmak glukagon sekreshכn, εn rεgεl di sεntri εnεji bεlε sεnta, bכt i de gi wan inovativ tritmεnt stratεji fכ di kכmprεhεnsiv mεnejmεnt fכ krכnik mεtabolik sik dεm tru di kכdivaskyul protεktiv ifekt εn pכtεnshal bεnεfit dεm fכ di sεntri nεv sistεm. i aplikeshכn pכtεnshal in mכltipכl sik εria dεm de kכnfכm di imכtant posishכn fכ GLP-1 rεsεptכr agonist dεm as kכr tritmεnt mεtכd in mכdan mεtabolik mεdisin.
▎ Sɔmari
di kכmbaynshכn fכ Cagrilintide εn Semaglutid (Cagrisema) sho signifyant sinagεstik ifekt dεm na di tritmεnt fכ fat εn tayp 2 mεtabolism mεlitus. dis kכmbaynshכn tεrapi de achy mכlti-dimεnshכnal rεguleshכn fכ apεtit, blכd glukכs mεtabolism, εn weit mεnejmεnt bay we i de tכk to di amylin εn GLP-1 rεsεpכta dεm wan tεm. di kagrilintayd de rεgεl tru dilay gεstrik εmpti εn sεntri satiety rεgulεshכn, we Semaglutid de inhεbit glukagon sekreshכn εn i de εnhans insulin sekreshכn. di sinagεstik ifekt fכ di tu de sכmtεm εnhans di ifekt dεm we di wet lכs εn blכd glukכs kכntrכl.
Klinik trayal data sho se Cagrisema (di kɔmbaynshɔn fɔ Cagrilintide 2.4mg ɛn Semaglutid 2.4mg) de mek pɔsin lɔs avɛrej wet we na 9.07% (wan absɔlɔb wet lɔs we na 9.11kg) insay di tritmɛnt tɛm we na 20 to 32 wik, we rili bɛtɛ pas di tritmɛnt we dɛn yuz Semaglutid 2.4mg wan tɛm insay di wik in wan [1] . Insay wan 32 wik, multicenter, double-blind, phase 2 klinik trial, di weit we di pasɛnt dɛn we dɛn trit wit CagriSema bin lɔs bin rili big pas di wan dɛn we dɛn trit wit Semaglutid ɔ Cagrilintide nɔmɔ.
di wet lכs na di CagriSema grup na bin -15.6%, dat na di Semaglutid grup na -5.1%, εn di wan na di Cagrilintide grup na -8.1% [2] . pan tap dat, Cagrisema de du fayn bak fכ ridyus glycated hemoglobin (HbA1c) εn impruv di kכdivaskyul risk indikεtכr dεm, we di risk fכ haypoglycemia rili lכw. Tru wan mכlti-target mεkanism, dis kכmbayn tritmεnt rεjim nכ de כnli optimiz mεtabolik paramita dεm bכt i de ridyus di risk fכ kכdivaskyul ivent dεm bכku bכku wan, we de gi mכr kכmprεhεnsiv tritmεnt opshכn fכ pasεn dεm we fat εn tayp 2 mεtabolism mεlitus.
Bɔt di pɔsin we rayt di buk
Di tin dɛn we wi dɔn tɔk bɔt, na ɔl di tin dɛn we Cocer Peptides dɔn du risach, ɛdit ɛn kɔmpilayt.
▎Sayteshɔn dɛn we gɛt fɔ du wit dis
[1] Dutta D, Nagendra L, Harish B. G., ɛn ɔda pipul dɛn. Efikεsi εn Sefty כf Cagrilintide nכmכ εn in kכmbaynshכn wit Semaglutid (Cagrisema) as Anti-Obesity Mεdikeshכn: Wan Sistεmatik Rivyu εn Mεta-Analysis[J]. Indian Jɔnal fɔ Ɛndokrinɔlɔji ɛn Mɛtabolism, 2024,28:436-444.DOI:10.4103/ijem.ijem_45_24.
[2] Frias JP, Deenadayalan S, Erichsen L, ɛn ɔda pipul dɛn. Efikεsi εn sef fכ kכ-administret wan tεm insay wik kagrilintayd 2·4 mg wit wan wik semaglutayd 2·4 mg in tayp 2 mεtabolism: wan mכltisεntr, randomizεd, dכbl-blaynd, aktv-kכntrכl, fεz 2 trayal[J]. Lancet, 2023,402 (10403):720-730.DOI:10.1016/S0140-6736(23)01163-7.
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.