Maz 10mg we yu de yuz

▎ Maz Struktrɔ

Sos: PubChem

Sikyɔn: AEGTFTSDVSSYLEGQAAKFIAWLVKGRG Mɔlikul Fɔmula: C 207H 317N 45O65 Molekyula Weyt: 4476g/mol CAS Nɔmba: 2259884-03-0 PubChem CID: 167312357, ɛn di ɔda wan dɛn Sinonim dɛn: GLXC-26803

▎ Maz Risach

Wetin na di risach bakgrɔn fɔ Maz?

Di impɔtant tin bɔt di wɔl fat ɛn sik dɛn we gɛt fɔ du wit am: 

Ovaweit ɛn fat dɔn bi big big prɔblɛm dɛn we de ambɔg pipul dɛn wɛlbɔdi na di wɔl mɔ ɛn mɔ. Di World Obesity Atlas bin tɔk se di nɔmba fɔ pipul dɛn we fat ɔlsay na di wɔl bin rich 764 milyɔn insay 2020 ɛn dɛn tink se i go go ɔp to 1 bilyɔn bay 2030. If pɔsin fat kin mek bɔku prɔblɛm dɛn wit wɛlbɔdi biznɛs, lɛk sik dɛn we de mek pɔsin in at ɛn di blɔd ɛn di tayp 2 mɛtabolism, we kin rili afɛkt di pɔsin in kwaliti fɔ liv ɛn di mɛrɛsin we i gɛt na di wɔl. Dis dɔn mek di wan dɛn we de stɔdi bɔt dis dɔn tray fɔ no aw fɔ trit pɔsin fayn, mɔ di nyu mɛrɛsin dɛn.

di divεlכpmεnt fawndeshכn fכ inkrεtin-bεys drog dεm: 

Frɔm we dɛn bin de tɔk bɔt inkrɛtin insay 1932, di risach we gɛt fɔ du wit dis dɔn de go bifo ɔltɛm. insay 1987, dεn bin no se GLP-1 na di kכl rεgεlεt fכ insulin sekreshכn na di pankrias, εn dεn bin divεlכp tritmεnt rεjim fכ tayp 2 mεtabolism we bεys pan inkrεtin. Insay 2005, dɛn bin apruv exenatide, di wɔl in fɔs GLP-1 riseptɔ agonist (GLP-1RA), fɔ makɛt, we lay wan sɔlid tiori ɛn prɛktikal fawndeshɔn fɔ di risach ɛn divɛlɔpmɛnt fɔ nyu inkrɛtin-bɛs drɔgs lɛk Maz. Maz na wan analכg fכ mamalian oxyntomodulin (OXM). as nyu jεnereshכn dual agonist we de tכk bכt GLP-1R εn GCGR, i gεt wan yunik dual-akshכn mεkanism εn brayt prכspεkt fכ di tritmεnt fכ weit lכs εn sik dεm we de rilet to am.

Wetin na di mɛkanism fɔ akshɔn fɔ Maz?

Agonistic ifekt pan di glukagon-layk pεptida-1 (GLP-1) rεsεptכr: 

GLP-1 na intestinal כmon we kin mek insulin sekreshכn εn inhibit glukagon sekreshכn insay wan we we dipεnd pan glukכs kכnsantreshכn, we de ridyus di glukכs lεvεl na di bכdi ^[1] . as GLP-1 risεptor agonist, Maz de miks di akshכn fכ GLP-1, we de εnhans insulin sekreshכn εn ridyus glukagon rilis, we de εp fכ rεgεl di bכdi glukכs. pan tap dat, di GLP-1 rεsεpכta agonist dεm kin delay di gεstrik εmpti, εnhans di satiety, εn rεdכks fכ it, we bεnεfit fכ kכntrכl di wet ^{[1, 2].}.

Agonistic ifekt pan di glukagon rεsεptכr: 

Glucagon kin mek di liva glycogen brok dכn εn gluconeogenesis, we kin mek di glukoz na di bכdi go כp. maz, bay we i de aktibכt di glukagon rεsεpכta, i kin rεgεl mכltipכl aspek dεm fכ di glukכs mεtabolism, we de achy fayn rεgulεshכn fכ di glukכs na di bכdi. Glucagon de mek bak lipolysis, i de ɛp fɔ ridyus di fat we de gɛda ɛn fɔ mek di bɔdi wet smɔl ^{[1, 2].}.

Rigyuletɔri ifɛkt pan blɔd prɛshɔn: 

Maz kin ridyus ɔl tu di sistolik ɛn diastolik blɔd prɛshɔn. na wan say, i de lכs bכdi prεshכn bay we i de rεgεl di glukכs εn lipid mεtabolism εn i de impruv di vaskulεr εndoteyl fכnshכn; na di כda say, i kin afekt di bכdi prεshכn rεguleshכn mεkanism dεm lεk di renin-angiotensin sistεm.

Wetin na di patikyula we aw Maz de mek pɔsin nɔ gɛt bɔku bɔku bɔdi?

rεgulεshכn fכ di glukכs na di bכdi εn mεtabolism: 

as dual agonist fכ di glukagon lεk pεptida-1 (GLP-1) εn glukagon rεsεpכta dεm, wan pan di mכltipכl fysiolojikal ifekt dεm fכ GLP-1 na fכ rεgεl di blכd glukכs lεvεl. I de mek insulin kɔmɔt, i de mek di glukagon nɔ kɔmɔt fayn, i de mek di glukɔs we de na di blɔd nɔ bɔku ^[1] , i de mek di bɛlɛ nɔ ɛmti, i de mek pɔsin satisfay, ɛn i de mek i nɔ it bɛtɛ tin fɔ it. di כda say, glukagon de mek di lipolysis εn di εnεji kכnsכm. fכ dat, Maz de aktibכt כl tu di rεsεpכta dεm εn de rεgεl di bכdi glukכs mεtabolism fכ achyv di wet lכs. Stɔdi dɔn sho se Maz kin ridyus di bɔdi wet, blɔd prɛshɔn (systolic ɛn diastolic), tɔtal kɔlɔstrel, triglisɛrɛyd, low-density lipoprotein, ɛn high-density lipoprotein lɛvɛl ^[3] , we sho se i kin mek pɔsin lɔs in wet ɛn impruv di mɛtabolik dizayd dɛn we gɛt fɔ du wit fat.

Influɛns pan di apɛtit ɛn di ɛnaji we pɔsin de it: 

Maz kin mek yu nɔ gɛt bɔku bɔku bɔdi bay we i de afɛkt di we aw yu want fɔ it ɛn di we aw yu de it ɛnaji. insay sɔm klinik trial, di patisipan dεm bin εkspiriεns gεstrointestinal riakshכn lεk dεkrεshכn apεtit afta dεn yuz Maz ^[3] . dis kin bi fכ di dayrekt akshכn we Maz de du pan di gεstrointestinal trakt כ tru rεguleshכn we di sεntri nεv sεstem de du. I nɔ mata di we aw dɛn de du am, we pɔsin nɔ want fɔ it ɛn di sayd ɛfɛkt dɛn we de na di bɛlɛ go mek i nɔ gɛt bɔku ɛnaji ɛn i go mek i nɔ gɛt bɔku bɔku bɔdi. apat frכm dat, Maz kin afekt di apεtit bay we i de rεgεl di nyurotransmit dεm εn di כmon dεm na di bren. fכ egzampl, GLP-1 kin akt pan di haypothalamus fכ rεgεl di apεtit εn εnεji bεlε ^[4]..

Wetin na di spεsifi k akshכn path dεm fכ Maz fכ rεgεl di bכdi glukכs?

Stimulation of insulin sekreshכn: 

glukagon lεk pεptida-1 (GLP-1) rεsεpכta agonist dεm kin mek insulin sekreshכn. as dual agonist fכ GLP-1 εn glukagon rεsεpכta dεm, Maz kin aktibכt di GLP-1 rεsεpכta fכ promp pankrεas aylet β sεl dεm fכ sekret insulin. Insulin na wan impɔtant ɔmon fɔ ridyus di glukɔs na di blɔd, we kin mek di sɛl dɛn tek glukɔs ɛn mek di glukɔs na di blɔd go dɔŋ ^[1]..

Inhibishכn fכ glukagon sekreshכn: 

di sem tεm, Maz kin akt pan di glukagon rεsεpכta fכ inhεbit glukagon sekreshכn. Glucagon ɛn insulin de agens dɛnsɛf fɔ rigul di glukɔs na di blɔd, ɛn fɔ ridyus di sekreshɔn we i de mek i fayn fɔ mek di glukɔs we de na di blɔd go dɔŋ ^{[1] .}.

Rεgulεshכn fכ glukכs mεtabolism: 

maz kin rεgεl di glukכs mεtabolism pan mכltipכl lεvεl dεm fכ εksεrt in haypoglycemic ifekt, lεk fכ afekt di glukכs mεtabolism na di liva, mכsul, εn adipos tisu dεm. insay di liva, i de ridyus di brok dכwn fכ di liva glycogen εn gluconeogenesis, we de dכn di prodakshכn fכ di bכdi glukכs; insay di mכsul tisu, i de protεkt di כptek εn yutilizeshכn fכ glukכs; insay adipos tisu, i de rεgεl di lipid mεtabolism, i de ridyus di rilis fכ fri fεt asid dεm, εn i de afekt di glukכs na di bכdi indaykt wan ^{[1, 3].}.

Influɛns pan di apɛtit ɛn di ɛnaji we pɔsin de it: 

stכdi dεn dכn fכnshכn se Maz kin ridyus di apεtit εn εnεji intayk, i kin bi bay we i de akt pan rεsεpכta dεm na di sεntri nεv sεstem εn rεgεl di apεtit signal path. if yu ridyus di it we yu de it, i kin mek di say we di glukɔs de kɔmɔt na di blɔd go dɔŋ ɛn i kin ɛp fɔ kɔntrol di glukɔs we de na di blɔd ^{[3, 5].}.

chenj frכm di beslayn insay di bכdi wet εn di wεst sεkכnfεnshכn.

a.Pεsεnt chenj frכm di bεslayn in bכdi wet ova tεm. b. Chenj frכm beslayn in bכdi wet ova tεm.

Sos:PubMed ^{[2] we dɛn pul am.}

Wetin na di aplikeshɔn dɛn fɔ Maz?

Tritmɛnt fɔ tayp 2 mɛtabolism: 

Wan randomized, double-blind, placebo-controlled Phase 2 trial sho se Maz, we na dual agonist we dɛn kin gi ɛvri wik fɔ glukagon-layk peptide 1 (GLP-1) ɛn glucagon riseptɔ, sho gud ɛfifikɛshɔn ɛn sef pan Chaynish pasɛnt dɛn we gɛt tayp 2 mɛtabolism ^[1]..

Aplikeshɔn fɔ lɔs wet: 

Risach pan pasɛnt dɛn we gɛt ɛn we nɔ gɛt mɛtabolism: Wan sistamat rivyu ɛn mɛta-analysis sho se Maz kin ridyus di bɔdi wet fɔ big pipul dɛn we gɛt ɔ we nɔ gɛt mɛtabolism fayn fayn wan ^[3] . Di risach inklud sɛvin randomized kɔntrol trial wit wan totɛl 680 patisipan dɛn. Di risal sho se we yu kɔmpia am wit di plasɛbo, Maz lid to wan mɔ signifyant ridyushɔn pan bɔdi wet (min difrɛns [MD] = -6.22%, 95% kɔnfidɛns intaval [CI]: -8.02% to -4.41%, I⊃2; = 90.0%) (Nalisa DL, 2024). Sabgrup ɛn mεta-rεgrεshכn analisis dεn fכnshכn se pasεn dεm we nכ gεt mεtabolism gεt mכr signifyant weit lכs, εn pasεn dεm we dεn trit fכ 24 wiks bin gεt mכr prominεnt weit rεdukshכn kכmpεr to dεn wan dεm we dεn trit fכ 12 - 20 wik ^[3]..

Aplikeshɔn fɔ Chaynish big pipul dɛn we gɛt bɔku bɔku bɔdi ɔ we fat pasmak: 

Wan mid-tɛm analisis fɔ wan randomized, tu-pat (lɔ doz te to 6mg ɛn ay doz 9mg), dabl-blaynd, plasɛbo-kɔntrol Faz 2 trayal we dɛn du pan Chaynish big pipul dɛn we gɛt ɔvaweit ɔ fat sho se Maz bin sef ɛn ifɛktiv insay dis pipul dɛn insay di 24 wik tritmɛnt tɛm, we briŋ kam signifyant ɛn klinikli mininful weit lɔs ^[2] . Insay di stɔdi, dɛn bin asaynd big pipul dɛn we gɛt ɔvawej (BMI ≥ 24 kg/m²) we gɛt haypafagia ɛn/ɔ at le wan kɔmɔrɔbiditi we gɛt fɔ du wit fat, ɔ big pipul dɛn we fat (BMI ≥ 28 kg/m²) fɔ gɛt Maz ɛvri wik pan dos dɛn we na 3mg, 4.5mg, 6mg ɔ wan we mach plasɛbo we dɛn kɔl plasɛbo. Di risal sho se frɔm di beslayn to di 24 wik, di min pasɛnt chenj na di bɔdi wet na bin -6.7% (standad mistek 0.7) na di 3mg Maz grup, -10.4% (0.7) na di 4.5mg grup, -11.3% (0.7) na di 6mg grup, ɛn 1.0% (0.7) na di plesbo grup. We yu kɔmpia am wit di plesibo, di tritmɛnt difrɛns bin de frɔm -7.7% to -12.3% (ɔl p < 0.0001) ^[2]..

fכ kכnklud, as inovativ dual-target agonist, tru mכltipכl mεkanism dεm lεk fכ rεgul di blכd glukכs, fכ protεkt fεt mεtabolism, εn inhibit apεtit, Maz kin ifektiv fכ impruv di blכd glukכs lεvεl fכ di pasεnshכn wit tayp 2 mεtabolism εn εp fכ fat pipul dεm fכ lכs wet. I de injεkt nyu vitality insay di tritmεnt fכ mεtabolik sik dεm εn dεn de εkspεkt fכ sכmtεm di globכl bכdi fכ fat εn sik dεm we de kam wit am.

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

Zhang B na wan ayli - kwalifay masta sabi bukman we gɛt fɔ du wit bɔku ɔganayzeshɔn dɛn we gɛt nem. Dɛn wan ya na Pekin Yuniɔn Mɛdikal Kɔlej, Chaynish Akademi fɔ Mɛdikal Sayns -Pekin Yuniɔn Mɛdikal Kɔlej, - Japan Friendship Ospital, Guizhou Ikwipmɛnt Mfg Politek, Shanghai Jiao Tong Yunivasiti, Yunivasiti Utara Malezya, Yingkou Instityut fɔ Tɛknɔlɔji, Zhejiang Yunivasiti, ɛn Peking Yuniɔn Mɛdikal Kɔlej Ospital. Dɛn kayn difrɛn institiushɔnal kɔnekshɔn ya de sho in brayt akademik ɛn risach bakgrɔn.

We i kam pan risach, Zhang B gɛt bɔku bɔku sɔbjɛkt kategori dɛn. In ɛkspɛriɛns de kɔba Ɛndokrinɔlɔji & Mɛtabolism, Jɛnɛral & Intanɛt Mɛdisin, Ɔnkɔlɔji, Kadiɔvaskyuɛl Sistɛm & Kadiɔlɔji, ɛn Rediolɔji, Nyuklia Mɛdisin & Mɛdikal Imej. Di wok we i de du pan dɛn tin ya de sho se i gɛt dip no ɛn i dɔn ɛp fɔ mek di mɛdikal sayɛns go bifo ɛn fɔ mek di we aw dɛn de kia fɔ wɛlbɔdi biznɛs bɛtɛ. Zhang B de na di list insay di rɛfrɛns fɔ saytayshɔn [1].

▎ Saytayshɔn dɛn we gɛt fɔ du wit dis

[1] Zhang B, Cheng Z, Chen J, ɛn ɔda pipul dɛn. Efikεsi εn Sefty כf Maz in Chaynish Pεshεnt wit Tayp 2 Mεtabolism: Wan Randomized, Double-Blind, Placebo-Controlled Phase 2 Trial[J]. Mεtabolism Kεr, 2024,47(1):160-168.DOI:10.2337/dc23-1287.

[2] Ji L, Jiang H, Cheng Z, ɛn ɔda pipul dɛn. A phase 2 randomized controlled trial of Maz in Chaynish ɔvaweit big pipul ɔ big pipul dɛn we gɛt fat[J]. Nature Komyunikeshɔn, 2023,14(1).DOI: 10.1038/s41467-023-44067-4.

[3] Nalisa D. L., Kuboia N, Dyab E, ɛn ɔda pipul dɛn. Efikεsi εn sef fכ Maz pan wεyt lכs bitwin dayabεtik εn nכn-dayabεtik pasεnshכn dεm: wan sεstεmatik rivyu εn mεta-analysis כf randomizεd kכntrold trayal dεm[J]. Frontiers in Ɛndokrinɔlɔji, 2024,15.

[4] Morris A. Unraveling nכvel weit lכs mεkanism dεm[J]. Nature Rivyu Ɛndokrinɔlɔji, 2020,16(7):343.DOI:10.1038/s41574-020-0374-4.

[5] Ji L, Gao L, Jiang H, ɛn ɔda pipul dɛn. Sefty ɛn ɛfifikɛshɔn fɔ wan GLP-1 ɛn glukagɔn riseptɔ dual agonist Maz (IBI362) 9 mg ɛn 10 mg insay Chaynish big pipul dɛn we gɛt ɔvawej ɔ fat: Wan randomiz, plasɛbo-kɔntrol, mɔltipɛl-asɛnd-dɔz faz 1b trayal[J]. Eklinikalmɛdisin, 2022,54:101691.DOI:10.1016/j.ɛklinm.2022.101691.

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.