Retatrud 40 mg

▎ Retatrutid Structure

Source: PubChem

Sequence: YA⊃1;QGTFTSDYSI-L⊃2;LDKK⁴AQA⊃1;AFIEYLLEGGPSSGAPPPS⊃3; Molecular Formula: C 221H 342N 46O68 Molecular Luj: 4731 g / mol CAS Nr .: 2381089-83-2 PubChem CID: 171390338 Synonyms: LY3437943

▎ Retatrutid Research

Kev tshawb fawb keeb kwm yav dhau rau Retatrutid yog dab tsi?

Lub ntiaj teb no muaj kev rog rog thiab ntshav qab zib hom 2 tseem nce ntxiv, ua rau muaj kev nyuaj rau pej xeem kev noj qab haus huv tseem ceeb. Cov tshuaj uas twb muaj lawm ib leeg lossis ob lub hom phiaj muaj kev txwv hauv kev ua tau zoo thiab kev nyab xeeb. Raws li txoj kev xav ntawm ntau lub hom phiaj kev tswj hwm kev tswj hwm ntawm lub plab zom mov insulin axis, kev tshawb fawb tau qhia txog lub luag haujlwm ntawm GLP-1, GIP, thiab glucagon hauv kev tswj hwm metabolic, muab lub hauv paus theoretical rau kev txhim kho ntau cov receptor agonists.

Tsim los ntawm kev paub txog kev tsim tshuaj thib ob lub hom phiaj ua ntej, cov kws tshawb fawb tau tsim thiab ua kom zoo dua Retatrutid raws li cov yam ntxwv ntawm cov qauv thiab cov kev taw qhia cov tswv yim ntawm cov receptors triple. Los ntawm kev ua haujlwm ib txhij GLP-1R, GIPR, thiab GCGR, nws ua tiav ntau lub zog glycemic tswj thiab txo qhov hnyav.

Yuav ua li cas yog lub mechanism ntawm kev txiav txim rau Retatrutid?

Receptor Agonism

Retatrutid ua haujlwm raws li triple receptor agonist tsom GLP-1, GCGR, thiab GIP receptors ^[1].

GLP-1 receptor agonism: GLP-1 yog incretin hormone secreted los ntawm txoj hnyuv L hlwb. Raws li kev khi rau GLP-1 receptors, Retatrutid txhawb nqa insulin tso tawm hauv cov piam thaj-concentration-dependent yam. Thaum lub sij hawm hyperglycemia, Retatrutid khi rau GLP-1 receptors, ua kom cov kev taw qhia qis qis uas ua rau cov kab mob pancreatic β-hlwb kom zais cov tshuaj insulin thiab txo cov ntshav qabzib. Nws kuj tseem inhibits glucagon secretion thiab txo qis cov piam thaj hauv siab, ua kom cov ntshav qabzib ruaj khov ntxiv. GLP-1 receptor agonism kuj tseem ncua lub plab zom mov, ua kom satiety, thiab txo cov zaub mov noj, pab tswj qhov hnyav ^[2].

GCGR receptor agonism: Glucagon feem ntau ua thaum lub sijhawm hypoglycemia kom nce qib ntshav qabzib. Retatrutid qhov kev txiav txim siab ntawm GCGR yog qhov nyuaj. Nyob rau hauv cov ntaub so ntswg adipose, nws txhawb lipolysis thiab tsub kom fatty acid oxidation, yog li pab txhawb kev siv zog. Hauv daim siab, qhov nruab nrab GCGR agonism tuaj yeem tswj cov txheej txheem zoo li gluconeogenesis, ua kom lub siab ua haujlwm metabolic. Qhov no tiv thaiv ntau dhau ntawm gluconeogenesis los ntawm kev ua rau hyperglycemia thaum tswj cov ntshav qabzib txaus kom ua tau raws li lub cev xav tau lub zog ^[1].

GIP receptor agonism: GIP, lwm yam tshuaj incretin, yog zais los ntawm K hlwb hauv duodenum thiab jejunum tom qab noj mov. Retatrutid's GIP receptor agonism txhim kho insulin secretion, sib koom ua ke nrog GLP-1 txhawm rau txhim kho kev tswj cov piam thaj. Hloov pauv, GIP receptor activation tuaj yeem cuam tshuam lipid metabolism thiab lub zog sib npaug. Brzozowska P txoj kev tshawb fawb qhia tias GIP txhawb nqa cov piam thaj thiab lipid synthesis hauv adipocytes. Txawm li cas los xij, raws li Retatrutid lub hwj chim, GIP signaling yog hloov kho kom zoo dua kev siv hluav taws xob ntau dua li tsuas yog txhawb nqa cov roj cia, yog li pab tswj qhov hnyav ^[1].

Daim duab 1 Retatrutid's mechanisms of action ^[3].

Kev tswj hwm ntawm cov txheej txheem metabolic

Kev tswj hwm lub zog Metabolism: Los ntawm kev ua kom peb lub receptors tau hais los saum no, Retatrutid ua tiav tswj cov metabolism hauv lub zog. Nws txhawb lipolysis, nce fatty acid nkag mus rau hauv mitochondria rau β-oxidation thiab txhawb zog siv nyiaj. Nws txo lipogenesis los ntawm inhibiting fatty acid uptake thiab triglyceride synthesis nyob rau hauv adipocytes, yog li hloov lub cev lub zog cia thiab tshuav nyiaj li cas los pab kom poob ceeb thawj. Hauv kev tshawb fawb txog tsiaj txhu thiab kev sim tshuaj los ntawm Jastreboff AM, Retatrutid kev tswj hwm tau nce kev siv hluav taws xob ntau ntxiv thiab txo qis lub cev rog cov ntsiab lus hauv cov rog rog ^[4].

Glucose Metabolism Regulation: Retatrutid modulates ntshav qabzib los ntawm ntau txoj hauv kev. Tshaj li stimulating insulin secretion ntawm GLP-1 thiab GIP receptor activation, nws cuam tshuam rau cov piam thaj hauv siab los ntawm kev tswj GCGR. Nws suppresses hepatic gluconeogenesis ntau dhau, txo cov piam thaj tso zis, thiab ib txhij txhim kho peripheral cov ntaub so ntswg glucose uptake thiab siv, yog li tswj cov ntshav qabzib ib txwm. Qhov no yog qhov tseem ceeb tshwj xeeb rau cov neeg mob rog rog uas muaj ntshav qab zib hom 2, tswj cov ntshav qabzib zoo thiab txhim kho cov mob ntshav qab zib ^[2].

Kev Tswj Xyuas Lub Siab: Hauv daim siab, Retatrutid tsis tsuas yog hloov pauv cov piam thaj metabolism, tab sis kuj cuam tshuam cov lipid metabolism. Nws txo qis triglyceride synthesis thiab tsub zuj zuj ntawm hepatic triglycerides, txhim kho hepatic steatosis, thiab tuav cov nqi kho mob rau cov kab mob uas tsis yog-alcoholic fatty siab (NAFLD). Hauv kev sim tshuaj uas koom nrog cov neeg koom nrog kev ua haujlwm tsis zoo ntawm cov kab mob metabolic cuam tshuam nrog cov kab mob rog rog (MDAFLD), Retatrutid txo qis cov rog rog hauv siab, ua kom pom nws cov txiaj ntsig zoo ntawm cov metabolism hauv hepatic ^[5].

 Cov teebmeem ntawm kev ua haujlwm ntawm plab hnyuv

Retatrutid ncua lub plab khoob los ntawm kev ua kom GLP-1 receptors. Lub plab zom mov qeeb qeeb ua rau lub sijhawm noj zaub mov nyob hauv lub plab, ua kom muaj kev txaus siab thiab txo qis kev noj zaub mov ntxiv. Nyob rau tib lub sijhawm, nws tuaj yeem cuam tshuam rau lub plab hormonal secretion thiab plab hnyuv motility, ntxiv regulating gastrointestinal digestion thiab assorption txheej txheem, yog li muaj kev cuam tshuam rau lub zog noj thiab lub cev hnyav ^[2].

Dab tsi yog qhov sib koom ua ke ntawm Retatrutid's agonistic teebmeem ntawm GLP-1, GCGR, thiab GIP receptors?

Synergy nyob rau hauv Zog Metabolism Regulation

Kev siv hluav taws xob ntau ntxiv: Ua kom GCGR txhawb nqa glycogenolysis thiab gluconeogenesis kom nce qib ntshav qabzib. Nws kuj tseem txhim kho kev siv hluav taws xob los ntawm kev ua kom cov lipid metabolism thiab txo qis kev noj zaub mov los ntawm qhov nruab nrab satiety. GLP-1R agonists txhawb nqa cov tshuaj insulin tso tawm thiab tawm dag zog cardioprotective thiab neuroprotective teebmeem, thaum tseem txo qis kev noj qab haus huv los ntawm kev ncua lub plab zom mov thiab txo qis qab los noj mov. Thaum GIPR ua rau hauv cov ntaub so ntswg adipose txhawb lipid tsub zuj zuj, nws lub hauv paus ua kom txo tau cov zaub mov noj thiab txo qhov hnyav nce. Retatrutid ib txhij tsom rau peb cov receptors no, tsim kom muaj kev sib npaug tshiab ntawm kev siv zog thiab kev siv nyiaj. Qhov no zoo dua ua tiav lub zog tsis txaus, yog li yooj yim rau kev poob phaus.

Kev tswj cov lipid metabolism: GCGR agonism txhim kho lipid metabolism, thaum GIPR ua rau hauv cov ntaub so ntswg adipose kuj cuam tshuam lipid metabolism. GLP-1R agonists tuaj yeem cuam tshuam ncaj qha rau lipid metabolism los ntawm cov txheej txheem xws li kev txhim kho insulin rhiab heev. Lawv cov synergistic ua haujlwm zoo dua tswj cov roj synthesis, tawg, thiab kev thauj mus los, txo cov rog thiab txhim kho lub cev rog. Piv txwv li, kev tshawb fawb hauv cov neeg mob rog tau pom tias tom qab siv Retatrutid rau ib lub sijhawm, lub cev rog feem pua ​​​​tso qis thiab lipid profile tau txhim kho rau qee qhov, qhia txog nws cov txiaj ntsig zoo hauv kev tswj cov roj metabolism ^[6].

Synergistic Effects hauv Glucose Regulation

Txhim kho Insulin Secretion: GLP-1R agonists txo cov ntshav qabzib los ntawm kev khi rau GLP-1 receptors thiab txhawb kev tso tawm insulin. GIP zoo ib yam ua rau cov kab mob pancreatic β-hlwb los tsim cov tshuaj insulin secretion zoo ib yam li cov neeg raug ntxias los ntawm kev noj haus. Retatrutid, uas ib txhij ua rau GLP-1R thiab GIPR, txhim kho insulin secretion, yog li txo qis cov ntshav qabzib ntau dua. Txawm hais tias GCGR feem ntau cuam tshuam nrog cov ntshav qabzib siab, nws cov teebmeem-xws li txhawb kev siv hluav taws xob- tuaj yeem ua rau tsis muaj zog rau cov piam thaj hauv lub cev thaum sib koom ua ke nrog cov receptors zoo li GLP-1R. Tsis tas li ntawd, kev siv ua ke ntawm GLP-1 thiab GCGR xaiv tau tawm tsam qhov kev pheej hmoo hyperglycemic tshwm sim los ntawm GCGR, ua kom muaj kev tswj hwm cov piam thaj ntau dua thiab muaj txiaj ntsig.

Regulating Glucose Homeostasis: Lub synergistic activation ntawm peb cov receptors txuas ntxiv tshaj li cov tshuaj insulin tso tawm kom suav nrog kev tswj hwm cov piam thaj hauv homeostasis. Los ntawm kev cuam tshuam cov piam thaj nce ntxiv, kev siv, thiab khaws cia thoob plaws ntau cov ntaub so ntswg nrog rau daim siab, nqaij, thiab adipose, Retatrutid tswj cov ntshav qabzib nyob rau hauv ib qho kev ruaj khov, tiv thaiv kev hloov pauv loj. Hauv kev tshawb fawb los ntawm Nicholls S cuam tshuam nrog cov neeg mob ntshav qab zib hom 2, Kev tswj hwm Retatrutid ua rau txo qis glycated hemoglobin qib, qhia txog nws qhov kev cuam tshuam zoo rau kev tswj glycemic mus sij hawm ntev thiab ua kom pom qhov cuam tshuam ntawm peb cov receptors hauv kev tswj cov piam thaj homeostasis ^[6].

Synergistic Activation of Signal Transduction Pathways

Kev Ua Haujlwm Zoo Tshaj Plaws: GLP-1R, GCGR, thiab GIPR feem ntau teeb liab los ntawm G (Gαs) cov proteins. Thaum Retatrutid ua rau peb cov receptors no, nws sib sau ua ke los ua kom muaj kev sib koom ua ke xws li cAMP-PKA txoj hauv kev. Txoj kev sib koom ua ke no txhim kho cov teeb liab transduction efficiency thiab potency, amplifying kev tswj cov teebmeem ntawm cellular metabolism thiab physiological functions.

Kev sib koom ua ke ntawm txoj kev sib txawv: Thaum sib koom txoj hauv kev, txhua tus neeg txais txiaj ntsig kuj tseem ua kom muaj kev sib txuas lus tshwj xeeb. Retatrutid modulates cov kev sib txawv no synergistically thaum lub sij hawm receptor activation, ua kom muaj kev sib koom ua ke ntawm cov txheej txheem metabolic.

Synergistic Regulation of Gastrointestinal Function

Influencing Gastrointestinal Hormone Secretion: GLP-1R agonists txhawb nqa GLP-1 secretion, thaum GIPR agonists tswj GIP tso tawm. Cov tshuaj hormones digestinal no ua lub luag haujlwm tseem ceeb hauv kev hloov pauv ntawm lub plab zom mov, kev zom zaub mov, thiab kev nqus. Los ntawm ib txhij ua rau ob qho tib si receptors, Retatrutid muab kev tswj hwm ntau dua ntawm kev tso cov tshuaj hormones hauv plab, yog li cuam tshuam rau kev ua haujlwm ntawm plab hnyuv. Nws tuaj yeem txo cov khoom noj sai sai los ntawm kev hloov pauv ntawm cov plab hnyuv siab raum thiab plab hnyuv, pab kom hnyav thiab tswj ntshav qabzib.

Txhim kho lub plab hnyuv Metabolic ib puag ncig: Los ntawm kev tswj cov kab mob hauv plab hnyuv, Retatrutid kuj txhim kho cov metabolism hauv ib puag ncig hauv plab hnyuv. Nws txhawb txoj kev loj hlob thiab cov metabolism ntawm cov kab mob hauv plab uas muaj txiaj ntsig zoo thiab hloov kho txoj hnyuv ua haujlwm. Cov kev hloov pauv no tuaj yeem cuam tshuam ntxiv rau lub cev tag nrho cov txheej txheem metabolic. Ua haujlwm synergistically nrog cov teebmeem ntawm lub zog metabolism thiab kev tswj cov ntshav qabzib, cov txheej txheem no sib sau ua ke rau kev kho cov teebmeem ntawm kev rog rog thiab cuam tshuam txog cov kabmob metabolic.

Cov ntawv thov ntawm Retatrutid yog dab tsi?

Kev kho mob rog

Qhov Tseem Ceeb Poob Qhov Teeb Meem: Ntau qhov kev sim tshuaj ntsuam xyuas pom tau tias Retatrutid qhov ua tau zoo hauv kev kho mob rog. Hauv Phase 2 ob qhov muag tsis pom kev, randomized, placebo-tswj sim los ntawm Jastreboff AM uas muaj 338 tus neeg laus, cov neeg koom tau txais Retatrutid txhua lub lim tiam ntawm kev sib txawv ntawm cov koob tshuaj lossis cov placebo rau 48 lub lis piam. Cov txiaj ntsig tau pom tias nyob rau lub lim tiam 24, pawg 1mg ua tiav qhov hnyav nruab nrab ntawm 7.2%, pawg 4mg ua ke poob 12.9%, pawg 8mg ua ke poob 17.3%, thiab 12mg pawg poob 17.5%, thaum pawg placebo poob tsuas yog 1.6%. Los ntawm lub lim tiam 48, pawg 1mg tau ua tiav qhov hnyav nruab nrab ntawm 8.7%, pawg 4mg ua ke poob 17.1%, pawg 8mg ua ke poob 22.8%, 12mg pawg poob 24.2%, thiab pawg placebo poob 2.1%. Ntawm cov neeg koom tau txais 4mg, 8mg, thiab 12mg Retatrutid, 92%, 100%, thiab 100% ua tiav 5% lossis ntau dua qhov hnyav, feem. 75%, 91%, thiab 93% ua tiav 10% lossis ntau dua qhov hnyav. thiab 60%, 75%, thiab 83% ua tiav 15% lossis ntau dua qhov hnyav, piv rau 27%, 9%, thiab 2% hauv pawg placebo. Cov ntaub ntawv no qhia meej txog Retatrutid qhov ua tau zoo hauv kev txo qhov hnyav rau cov neeg mob rog ^[4].

Kev kho mob ntshav qab zib hom 2

Glycemic Control Efficacy: Kev tshawb fawb los ntawm Lopez DC thiab al. qhia Retatrutid zoo cuam tshuam glycemic tswj hauv cov neeg mob ntshav qab zib hom 2. Hauv kev sim nrog 353 tus neeg koom, Retatrutid txo glycated hemoglobin (HbA1c) los ntawm 1.64% piv rau cov placebo. Qhov no qhia tau hais tias Retatrutid qhov ua tau zoo hauv kev txo cov ntshav qabzib hauv cov neeg mob ntshav qab zib hom 2, yog li pab txhawb kev kho mob tau zoo ^[7].

Combined Mechanism Advantage: Retatrutid ua rau ntau tus receptors, muab qhov zoo dua qub ntawm ib leeg-receptor agonists los ntawm nws cov txheej txheem ua ke agonist. Nws tsis tsuas yog txo cov ntshav qabzib los ntawm kev tsim cov tshuaj insulin secretion, tab sis kuj tseem txhim kho cov tshuaj insulin, ua rau lub cev cov hlwb siv cov tshuaj insulin zoo dua rau kev tswj hwm glycemic. Nws cov txiaj ntsig txo qhov hnyav ntxiv txhim kho cov txheej txheem metabolic hauv cov neeg mob ntshav qab zib hom 2, vim tias rog rog yog qhov tseem ceeb rau tus mob thiab kev poob phaus ua rau muaj kev tswj hwm ntshav qabzib zoo dua ^[5].

Kev kho mob uas tsis yog-Alcoholic Fatty Liver Disease

Txo cov rog rog hauv daim siab: Retatrutid tau pom tias muaj peev xwm txo cov rog rog hauv cov neeg mob uas muaj cov kab mob metabolic tsis ua hauj lwm cuam tshuam nrog cov kab mob fatty siab (MDAFLD) thiab daim siab rog cov ntsiab lus ≥10%. Hauv kev sib tw randomized, ob-dig muag, kev sim tshuaj placebo, 98 tus neeg koom tau raug xaiv kom tau txais kev txhaj tshuaj subcutaneous txhua lub lim tiam ntawm Retatrutid (1mg, 4mg, 8mg, lossis 12mg) lossis placebo rau 48 lub lis piam. Cov txiaj ntsig tau pom tias nyob rau lub lim tiam 24, qhov kev hloov pauv ntawm cov rog hauv siab txheeb ze rau cov hauv paus ntsiab lus yog -42.9% hauv pawg 1mg, -57.0% hauv pawg 4mg, -81.4% hauv pawg 8mg, thiab -82.4% hauv pawg 12mg, piv rau +0.3% hauv pawg placebo. Cov kev tshawb pom no qhia tias Retatrutid txo qis cov roj ntsha hauv siab, ua kom pom qhov muaj peev xwm kho tau rau cov kab mob tsis muaj dej cawv fatty siab ^[8].

Txhim kho Hepatic Metabolic Function: Retatrutid txhim kho daim siab metabolic muaj nuj nqi los ntawm kev tswj lub zog thiab lipid metabolism. Nws txhawb kev oxidation thiab rhuav tshem cov rog rog, txo cov rog hauv daim siab, hloov cov lus teb inflammatory thiab oxidative kev ntxhov siab nyob rau hauv daim siab, thiab ua rau muaj qee yam inhibitory cuam tshuam rau kev loj hlob ntawm NAFLD, yog li tiv thaiv cov neeg mob lub siab noj qab haus huv.

Xaus

Raws li ib tug triple receptor agonist ntawm GLP-1R / GIPR / GCGR, Retatrutid exerts metabolic regulatory teebmeem los ntawm ntau lub hom phiaj synergistic mechanism. Nws cov teebmeem encompass activating GLP-1R los suppress qab los noj mov thiab ncua lub plab khoob, yog li txo lub zog kom tsawg; activating GIPR los txhim kho insulin secretion thiab txhim kho cov tshuaj insulin rhiab heev; thiab ua kom GCGR txhawb kev lipolysis thiab kev siv hluav taws xob thaum tswj cov piam thaj hauv siab thiab lipid metabolism kom txo cov rog. Qhov kev sib koom ua ke triple no ua tiav cov txiaj ntsig zoo suav nrog kev tswj hwm glycemic muaj zog, txo qhov hnyav, thiab txhim kho lipid thiab cov rog rog metabolism. Nws cov txiaj ntsig tseem ceeb yog nyob rau hauv kev kho mob rog, ua kom tau txais koob tshuaj raws li qhov hnyav txo nrog qhov siab tshaj 48 lub lis piam poob ntawm 24.2%. Rau hom 2 mob ntshav qab zib mellitus, nws txo qis glycated hemoglobin thiab txhim kho glycemic homeostasis. Nyob rau hauv metabolic dysfunction-ssociated fatty daim siab kab mob, nws ho txo ​​cov roj hepatic cov ntsiab lus, qhia tau hais tias muaj peev xwm ua tau zoo nyob rau hauv ntau yam metabolic ntshawv siab.

Hais Txog Tus Sau

Cov ntaub ntawv hais saum toj no yog txhua yam tshawb fawb, kho thiab sau los ntawm Cocer Peptides.

Scientific Journal Author

Arun J. Sanyal yog kws kho mob hepatologist thiab kws tshawb fawb tshwj xeeb hauv cov kab mob siab, tshwj xeeb tshaj yog cov kab mob tsis muaj dej cawv fatty siab (NAFLD) thiab tsis muaj cawv steatohepatitis (NASH). Nws koom nrog Virginia Commonwealth University Tsev Kawm Ntawv Tshuaj Kho Mob, qhov chaw uas nws tau ua tus kws qhia ntawv txij li xyoo 1989. Sanyal tau sau kwv yees li 1,000 cov ntawv tshaj tawm hauv cov ntawv tshaj tawm xws li Cell Metabolism, Nature Medicine, The New England Journal of Medicine, thiab The Lancet. Nws txoj haujlwm tau raug suav hais tias ntau dua 104,000 lub sijhawm, qhia txog nws qhov cuam tshuam tseem ceeb hauv thaj chaw hepatology. Nws tau txais nyiaj tsis tu ncua los ntawm National Institutes of Health txij li xyoo 1995 thiab yog tus kws tshawb fawb tseem ceeb ntawm plaub qhov nyiaj pabcuam NIH. Sanyal kuj tau lees paub rau nws cov thawj coj hauv kev tshawb fawb soj ntsuam thiab nws txoj kev koom tes rau kev txhim kho cov tswv yim kho mob rau cov kab mob siab. Arun J. Sanyal tau teev nyob rau hauv qhov kev siv ntawm cov ntaub ntawv pov thawj [5].

▎ Cov Lus Qhia Tseem Ceeb

[1] Brzozowska P, Frańczuk A, Nowińska B, Makłowicz A, Palacz KA, Lenartowicz I. Retatrutid - revolutionary nyuam qhuav tsim GLP agonist - ntaub ntawv tshuaj xyuas. Zoo hauv Sport 2024. https://api.semanticscholar.org/CorpusID: 271031379.

[2] Doggrel SA. Retatrutid qhia kev cog lus hauv kev rog rog (thiab ntshav qab zib hom 2). Cov Kws Tshaj Lij Tshaj Tawm Txog Kev Tshawb Fawb Tshuaj 2023; 32(11): 997-1001.DOI: 10.1080/13543784.2023.2283020.

[3] Katsi V, Koutsopoulos G, Fragoulis C, Dimitriadis K, Tsioufis K. Retatrutid—A Game Changer in Obesity Pharmacotherapy. Biomolecules 2025; 15(6).DOI: 10.3390/biom15060796.

[4] Jastreboff AM, Kaplan LM, Frías JP, et al. Triple-hormone-Receptor Agonist Retatrutid for Obesity - Theem 2 Kev sim. New England Journal of Medicine 2023; 389(6): 514-526. DOI: 10.1056/NEJMoa2301972.

[5] Sanyal AJ, Kaplan LM, Frias JP, et al. Triple Hormone receptor agonist retatrutide rau metabolic dysfunction-associated steatotic siab kab mob: randomized theem 2a sim. Ntuj Tshuaj 2024; 30: 2037-2048. https://api.semanticscholar.org/CorpusID:270378167.

[6] Nicholls S, Pirro V, Lin Y, et al. Triple-hormone receptor agonist retatrutide ua rau muaj kev txhim kho lipoprotein thiab apolipoprotein profiles hauv cov neeg koom nrog rog lossis rog. European Heart Journal 2024; 45(Supplement_1): ehae666-ehae1501.DOI:10.1093/eurheartj/ehae666.1501.

[7] Lopez DC, Pajimna JT, Milan MD, et al. 7792 Kev Ua Tau Zoo ntawm Retatrutid rau Kev Txo Qhov Nyuaj thiab Nws Cov Teebmeem Cardiometabolic Ntawm Cov Neeg Laus: Kev Ntsuam Xyuas Txheej Txheem thiab Kev Ntsuas Meta. Phau ntawv Journal of the Endocrine Society 2024; 8(Supplement_1): bvae163-bvae749.DOI: 10.1210/jendso/bvae163.749.

[8] Naeem M, Imran L, Banatwala U. Unleashing lub hwj chim ntawm retatrutide: Ib tug muaj peev xwm triumph tshaj rog thiab rog: Ib tsab ntawv. Kev Tshawb Fawb Txog Kev Noj Qab Haus Huv 2024; 7(2): e1864.DOI: 10.1002/hsr2.1864.

Tag nrho cov kab lus thiab cov ntaub ntawv ntawm cov khoom lag luam muab rau ntawm lub vev xaib no tsuas yog rau cov ntaub ntawv tshaj tawm kev tshaj tawm thiab cov hom phiaj kev kawm.  

Cov khoom muab rau hauv lub vev xaib no yog npaj tshwj xeeb rau kev tshawb fawb hauv vitro. Kev tshawb fawb hauv vitro (Latin: * hauv iav *, lub ntsiab lus hauv iav) yog ua los ntawm tib neeg lub cev. Cov khoom no tsis yog tshuaj, tsis tau txais kev pom zoo los ntawm US Food and Drug Administration (FDA), thiab yuav tsum tsis txhob siv los tiv thaiv, kho, lossis kho txhua yam mob, kab mob, lossis mob. Nws raug txwv nruj raws li txoj cai los qhia cov khoom no rau hauv tib neeg lossis tsiaj lub cev hauv txhua daim ntawv.