Kagrilintayd 10mg

▎ Di Strukchɔ we di Kagrilintayd gɛt

▎ Risach bɔt Kagrilintayd

Wetin na di risach bakgrɔn fɔ Cagrilintide?

cagrilintide na dual amylin εn kalsitonin rεsεptכr agonist (DACRA) we dεn divεlכp bays pan di strכkchכ fכ amylin. di pankrεas aylet β sεl dεm de kכl amylin εn i de wok insay kכnsεt wit insulin fכ du difrεn fysiolojikal fכnshכn dεm. i kin mek yu fil fכ satiet εn ridyus di it we yu de it, mεntal wan bay we i de aktibכt di rεsεpכta dεm na di εria postrema na di bεs fכ di fכs vεntrikl. di nyural signal dεm de transmit to di fכbren tru di nyuklios fכ di solitary trakt εn dεn kin transmit bak to di lateral haypothalamic εria εn כda nyuklia grup dεm tru di lateral parabrachial nyuklios, we de mek di satiety sεntr εn inhεbit fכ it ^[1] . amylin kin rεgεl di glukכs homכstasis bak bay we i de inhεbit di sekreshכn fכ insulin εn glukagon fכ mεnten di blכd glukכs lεvεl stebul ^[2] . in mεkanism dεm inklud dayrekt ifekt pan pankrεas aylet α sεl dεm εn indaykt rεguleshכn fכ glukagon sekreshכn tru nyural signal dεm na di haypothalamus. pan di sik pipul dεm we gεt mεtabolism, di dεstrukshכn fכ di β sεl dεm de mek di amylin sekreshכn dכn. amylin de tek pat pan di rεguleshכn fכ glukכs homכstasis bay we i de inhεbit gastric εmpti εn postprandial hεpatik glukכs prodakshכn, we de ridyus di postprandial bכdi glukכs fכlt. I kin mek bak di gastric ɛmti, i kin mek di gastrointestinal peristalsis nɔ apin, i kin mek di it fɔ lɔng tɛm, ɛn i kin mek di glukɔs na di blɔd nɔ go ɔp bad bad wan. כltu, di sכt haf-layf fכ nεchכral amylin de limited in klinik aplikεshכn. Pan ɔl we pramlintide de as adjuvant drɔg, i nid fɔ tek tri injɛkshɔn insay wan de, we nɔ kin izi ɛn i kin mek dɛn nɔ fala di lɔ fayn fayn wan ^[3] . Fɔ adrɛs dis prɔblɛm, dɛn bin mek Cagrilintide. di risach εn divεlכpmεnt we i de du de bays pan dip כndastandin fכ di fysiolojikal fכnshכn dεm fכ nεchכral amylin, we de aim fכ miks in mεkanism fכ akshכn we i de impruv di stebiliti εn lכng-aktin prכpati dεm fכ di dכg fכ mit klinik nid dεm.

Wetin na Kagrilintayd?

Cagrilintide na nyu lכng-akt amylin analכg wit big pכtεnshal, we dεn dכn sho fכ di fכs ifektiv fכ trit fכ fat εn mεtabolism. i dכn lipidεt εn i gεt stebul εn lכng-akt kכntribyushכn dεm ^[3] . amylin de kכ-rilis wit insulin bay pankrεas β sεl dεm εn i de mek yu fil fכ sati bay we i de akt pan di homכstatik εn gladi rijyכn dεm na di bren. As analɔg, Cagrilintide kin falamakata dis ifɛkt, we de mek pɔsin sati fɔ ɛp fɔ kɔntrol di bɔdi wet. di sem tεm, as dual amylin εn kalsitonin rεsεptכr agonist (DACRA), i de kכmכt frכm di amylin bakbon εn i gεt wan yכnik mεkanism insay mεtabolik rεguleshכn.

Structural Model fɔ Kagrinlintayd

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Wetin na di rilayt aplikeshɔn dɛm fɔ Cagrilintide?

Insay klinik trial, Cagrilintide dɔn ajɔst fayn fayn rizɔlt fɔ mek pɔsin lɔs in wet. Fɔ ɛgzampul, insay wan multicenter, randomized, double-blind, placebo-controlled, ɛn active comparator Fase 2 dose-finding trial, we dɛn kɔmpia wit di plasɛbo grup, di avɛrej pasɛnt we di wet lɔs frɔm di beslayn insay ɛni doz grup fɔ Cagrilintide (0.3 - 4.5 mg) (6.0% - 10.8%) bin ay pas di wan we de na di plasɛbo grup (3.0%). di weit lכs na di 4.5 mg grup bin tu bכku pas di wan na di liraglutide 3.0 mg grup (10.8% vs. 9.0%), we sho se i kin bi wan ifektiv opshכn fכ weit mεnejmεnt ^[4] . di kagrilintayd gεt difrεnt bכt rilayt mεkanism fכ akshכn we yu kכmpεr wit di GLP-1 rεsεptכr agonist semaglutide. semaglutid de ridyus di apεtit, i de mek insulin sekreshכn bכku, εn i de delay di gεstrik εmpti bay we i de akt pan di GLP-1 rεsεpכta dεm na di haypothalamus, we Cagrilintide de ridyus di apεtit mכr bay we i de aktibכt di amylin rεsεpכta. di kכmbayn yus fכ di tu kin prodyuz wan supεrimכz ifekt, we kin bכku bכku wan εnhans di weit lכs ifekt ^[5] . We wi tink bɔt di kɔmplisiti fɔ fat, dis kɔmbayn tritmɛnt na rizin ɛn ifektiv strateji.

pan di sik pipul dεm we gεt tayp 2 mεtabolism, Cagrilintide dεn dכn sho bak gud bכdi glukכs kכntrכl abiliti. Klinik stכdi dεn sho se i gεt gud stεbiliti εn ifektiv fכ trit fכ fat εn tayp 2 mεtabolism. fכ egzampl, insay wan klinik trial pan pasεn dεm wit tayp 2 mεtabolism, di kכmbayn yus כf Cagrilintide εn di GLP-1 rεsεptכr agonist semaglutide sho gud bכdi glukכs kכntrכl εn weit lכs ifekt ^[6] . Wan ɔda trayal sho bak se i gud tolɛrabiliti ɛn sef we dɛn yuz am in wan ɔ in kɔmbayn wit semaglutide ^[6] , bikɔs di stebiliti fɔ di drɔg gɛt fɔ du wit in tolɛrabiliti ɛn sef.

Apat frɔm dat, dɛn dɔn telɛret Cagrilintide fayn fayn wan insay klinik trial dɛn. Insay di Faz 2 doz-fayndin trayal, di pɔrmanent diskɔntinyu rɛt na ɛni tritmɛnt grup bin fiba, mɔs bikɔs ɔf di bad tin dɛn we apin. Bɔt di bad tin dɛn we kin apin mɔ na di prɔblɛm dɛn we kin apin na di bɛlɛ ɛn di riakshɔn dɛn we kin apin na di say we dɛn injɛkshɔn, ɛn bɔku pan dɛn na bin smɔl to mɔdaret. Insay wan randomized, kɔntrol Faz 1b trayal, di kɔmbayn tritmɛnt fɔ Cagrilintide ɛn 2.4 mg semaglutide sho bak gud tolerabiliti ɛn sef ^[7] . Dɛn nid fɔ du big ɛn lɔng tɛm trayal dɛn tumara bambay fɔ mek dɛn ebul fɔ no gud gud wan aw dis kɔmbayn tritmɛnt go wok ɛn sef.

Cagrilintide de briŋ nyu op fɔ di tritmɛnt fɔ fat ɛn tayp 2 mɛtabolism. I de gi nyu tritmɛnt opshɔn fɔ di wan dɛn we fat, mɔ di wan dɛn we nɔ de ansa fayn to layf stayl intavɛnshɔn ɛn we nɔ fayn fɔ bariatric ɔpreshɔn. di yunik mεkanism we i de du de gi nyu aydia εn mεtכd fכ trit fכ fat, εn i kin gεt mכr advantej pas tradishכnal weit lכs drog dεm (D'Ascanio AM, 2024). di saksesful kes fכ di kכmbayn yus כf Cagrilintide εn semaglutide (CagriSema) sho se mכlti-target kכmbayn tritmεnt na wan ifektiv stratεji fכ impruv di tritmεnt rεspכns fכ fat ^[6] . dis mכdel de gi nyu paradaym fכ di mεnejmεnt fכ fat εn i de bכn bak signifyant mεtabolik improvεmεnt to pasεn dεm wit tayp 2 mεtabolism.

fכ kכnklud, as nכvel lכng-aktin amylin analכg, Cagrilintide gεt signifyant pכtεnshal fכ weit lכs εn blכd glukכs kכntrכl. i de aktibכt di satiety signal path bay we i de miks di akshכn fכ amylin εn i de rεgεl mεtabolism as dual rεsεpכta agonist. Klinik trial dεm dכn sho se Cagrilintide, in wan כ we dεn kכmbayn am wit semaglutide, kin ridyus di bכdi wet bכku bכku wan εn dεn kin tכlerεt am fayn fayn wan. Apat frɔm dat, i dɔn sho bak gud blɔd glukɔs kɔntrol abiliti pan pasɛnt dɛn we gɛt tayp 2 mɛtabolism, we de gi nyu tritmɛnt opshɔn fɔ di tritmɛnt fɔ fat ɛn mɛtabolism, we de ful di gap we de na di tritmɛnt rijim dɛn we de naw, mɔ fɔ di pasɛnt dɛn we nɔ de ansa fayn to layf stayl intavɛnshɔn ɛn we nɔ fayn fɔ ɔpreshɔn. in mכlti-target tritmεnt stratεji de gi nyu aydia fכ di mεnejmεnt fכ mεtabolik sik dεm.

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.

Sayɛns Jɔnal Author

Dɔktɔ D. C. W. Lau na prɔfɛsɔ na di Kaming Skul fɔ Mɛdisin, na di Yunivasiti na Kalgari, insay Kanada. In risach intɛres dɛn de kɔba ɛndokrinɔlɔji ɛn mɛtabolism, jenɛral ɛn intanɛnt mɛrɛsin, kadiɔvaskyuɛl sistɛm ɛn kadiɔlɔji, pɔblik wɛlbɔdi, envayrɔmɛnt ɛn ɔkupeshɔnal wɛlbɔdi, ɛn bak ɔnkɔlɔji. I gɛt pozishɔn bak wit Albata Ɛlth Sɛvis (AHS) ɛn Ɔbisiti Kanada ɛn i de wok na di Julia McFarlane Mɛtabolism Risach Sɛnta. Dɔktɔ Lau gɛt bɔku ɛkspiriɛns pan di fild dɛm fɔ mɛtabolism ɛn ɔbisiti risach, wit in wok we dɛn dɔn pablish na akademik jɔnal dɛm lɛk di Canadian Journal of Metabolism. Dכkta DCW dεn list am na di rεfrεns fכ saytεshכn [4].

▎ Saytayshɔn dɛn we gɛt fɔ du wit dis

[1] Hansen KE, Murali S, Chaves IZ, ɛn ɔda pipul dɛn. Glycomacropeptide Impacts Amylin-Mediated Satiety, Postprandial Markers of Glucose Homeostasis, ɛn di Fekal Maykrobayɔm insay Ɔbis Pɔstmɛnɔpɔz Uman dɛn[J]. J ɔ rnal ov Nutrishɔn, 2023,153(7):1915-1929.DOI:10.1016/j.tjnut.2023.03.014.

[2] Ling W, Huang Y, Qiao Y, ɛn ɔda pipul dɛn. Human Amylin: Frɔm Patɔlɔji to Fisiɔlɔji ɛn Famakɔlɔji[J]. Kɔrɛnt Protɛin & Pɛptid Sayns, 2019,20(9):944-957.DOI:10.2174/ 13892037206 66 19032811183 3.

[3] Kruse T, Hansen J L, Dahl K, ɛn ɔda pipul dɛn. Divεlכpmεnt כf Cagrilintide, wan Lכng-Aktin Amylin Analog[J]. J ɔ rnal ov M ɛ d ɛ sinal K ɛ m ɛ st ɛ r, 2021,64(15):11183-11194.DOI: 10.1021/acs.jmedchem.1c00565.

[4] Lau D. C. W., Erichsen L., Fransisko A. M., ɛn ɔda pipul dɛn. wan tεm insay di wik cagrilintide fכ weit mεnejmεnt in pipul dεm we gεt כvaweit εn fat: wan mכltisεntr, randomizεd, dכbl-blaynd, plasεbo-kכntrol εn aktv-kכntrol, dכz-fayndin fεz 2 trayal[J]. Lancet, 2021,398(10317):2160-2172.DOI:10.1016/S0140-6736(21)01751-7.

[5] D'Ascanio AM, Mullally JA, Frishman W H. Cagrilintide: Wan Lɔng-Aktin Amylin Analɔg fɔ di Tritmɛnt fɔ Ɔbisiti[J]. Kadioloji in Rivyu, 2024,32(1):83-90.DOI:10.1097/CRD.0000000000000513.

[6] Frias JP, Deenadayalan S, Erichsen L, ɛn ɔda pipul dɛn. Efikεsi εn sef fכ kכ-administret wan tεm wik kagrilintayd 2.4 mg wit wan wik semaglutayd 2.4 mg in tayp 2 mεtabolism: wan mכltisεntr, randomizεd, dכbl-blaynd, aktv-kכntrol, fεz 2 trayal[J]. Lancet, 2023,402(10403):720-730.DOI:10.1016/S0140-6736(23)01163-7.

[7] Enebo LB, Berthelsen KK, Kankam M, ɛn ɔda pipul dɛn. Sefty, tolerabiliti, famakokinɛtiks, ɛn famakodaynamiks fɔ kɔnkɔmit administreshɔn fɔ bɔku dos dɛn fɔ kagrilintayd wit sɛmaglutayd 2.4 mg fɔ wet mɛnejɛmɛnt: wan randomiz, kɔntrol, faz 1b trayal[J]. Lancet, 2021,397(10286):1736-1748.DOI:10.1016/S0140-6736(21)00845-X.

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.