Exenatide Txhaj

Shaanxi BLOOM Tech Co., Ltd. yog ib qho ntawm cov tuam ntxhab thiab cov muag khoom ntawm exenatide txhaj tshuaj hauv Suav teb. Txais tos rau kev lag luam wholesale bulk zoo exenatide txhaj rau muag ntawm no los ntawm peb lub hoobkas. Kev pabcuam zoo thiab tus nqi tsim nyog muaj.

Lub ntsiab feem ntawmExenatide Txhajyog Exenatide, ib qho khoom tsim peptide uas muaj 39 amino acids uas ua zoo ib yam li endogenous glucagon zoo li peptide-1 (GLP-1). Cov tshuaj excipients muaj xws li mannitol, sodium acetate trihydrate, meta cresol, glacial acetic acid, thiab dej txhaj tshuaj, uas tsis muaj xim thiab ntshiab kua. Nws cov qauv tshuaj yog complex, nrog ib tug molecular mis ntawm C184H282N50O60S thiab molecular hnyav txog li 4186.6.

 

Peb Cov Khoom Muag Khoom

 

Exenatide / Exenatide acetate COA

Certificate of Analysis
Compound npe	Exenatide / Exenatide acetate
Qib	Pharmaceutical qib
CAS Nr.	141732-76-5
Ntau	15g
Ntim txheem	PE hnab + Al foil hnab
Chaw tsim tshuaj paus	Shaanxi BLOOM TECH Co., Ltd
Ntau No.	202601090060
MFG	Peb 9, 2026
EXP	Peb 8, 2029
Qauv
Yam khoom	Enterprise txheem	Kev txheeb xyuas qhov tshwm sim
Qhov tshwm sim	Dawb los yog yuav luag dawb hmoov	Ua raws
Cov ntsiab lus dej	Tsawg dua lossis sib npaug li 5.0%	0.50%
Poob rau ziab	Tsawg dua lossis sib npaug li 1.0%	0.40%
Hnyav Hlau	Pb Tsawg dua lossis sib npaug li 0.5ppm	N.D.
	Tsawg dua lossis sib npaug li 0.5ppm	N.D.
	Hg Tsawg dua lossis sib npaug li 0.5ppm	N.D.
	Cd Tsawg dua lossis sib npaug li 0.5ppm	N.D.
Purity (HPLC)	Ntau dua lossis sib npaug li 99.0%	99.90%
Ib qho impurity	<0.8%	0.58%
Tag nrho microbial suav	Tsawg dua lossis sib npaug li 750cfu / g	170
E. Coli	Tsawg dua lossis sib npaug li 2MPN / g	N.D.
Salmonella	N.D.	N.D.
Ethanol (los ntawm GC)	Tsawg dua lossis sib npaug li 5000ppm	400ppm ua
Cia	Khaws rau hauv qhov chaw kaw, tsaus, thiab qhuav hauv qab 2-8 degree

Raws li thawj glucagon zoo li peptide-1 (GLP-1) receptor agonist pom zoo rau kev lag luam hauv ntiaj teb,Exenatide TxhajNws muaj ib qho ntawm nws cov tshuaj pharmacological tseem ceeb rau tshwj xeeb inhibit qhov txawv txav ntawm glucagon hauv cov neeg mob ntshav qab zib hom 2, uas kuj yog ib qho ntawm cov txheej txheem tseem ceeb kom ua tiav cov piam thaj kom raug thiab txo cov ntshav qabzib hloov pauv. Raws li qhov tseem ceeb ntawm glucocorticoid hauv lub cev, glucagon muaj qhov tsis txaus ntseeg hauv cov neeg mob ntshav qab zib hom 2 (kev tso tawm ntau dhau ntawm lub plab khoob thiab tom qab noj mov, thiab txo qis rhiab heev rau kev tswj hwm cov piam thaj hauv ntshav), uas ua rau cov ntshav qabzib ntau ntxiv thiab cov ntshav qabzib homeostasis tsis txaus, thiab yog ib qho tseem ceeb ntawm cov kab mob pathological uas ua rau hyperglycemia.

Glucagon yog peptide hormone synthesized thiab secreted los ntawm pancreatic islet alpha hlwb. Nws yog tsim los ntawm 29 amino acids thiab muaj qhov hnyav molecular ntawm kwv yees li 3485 Da. Ua ke nrog insulin, nws tsim "bidirectional regulatory system" rau kev tswj cov ntshav qabzib homeostasis hauv lub cev. Its core physiological function is to increase blood glucose levels to maintain energy supply during fasting and stress states. Cov txheej txheem tshwj xeeb ntawm kev nqis tes ua yog feem ntau cuam tshuam hauv peb yam hauv qab no:

Txhawb nqa cov piam thaj hauv siab: Qhov no yog qhov tseem ceeb ntawm kev ua haujlwm ntawm glucagon. Tom qab khi rau glucagon receptors nyob rau saum npoo ntawm daim siab hlwb, glucagon ua rau txoj hauv kev hauv lub cev, txhawb kev ua haujlwm ntawm glycogen hauv lub siab (hloov lub siab khaws glycogen rau hauv qabzib) thiab gluconeogenesis (synthesizing qabzib los ntawm cov khoom tsis qab zib xws li lactate, pyruvate, thiab cov kua qaub hauv siab), thiab nce cov piam thaj hauv siab. Nyob rau hauv ib txwm muaj lub cev muaj zog, qhov tso tawm ntawm glucagon nce me ntsis ntawm lub plab khoob, tswj hwm cov ntshav qabzib ceev hauv qhov qub (3.9-6.1 mmol / L) kom tsis txhob muaj ntshav qab zib.

Kev tswj cov roj metabolism: Glucagon tuaj yeem txhawb kev tawg ntawm cov ntaub so ntswg adipose, tso cov roj fatty acids thiab glycerol. Fatty acids yog oxidized thiab tawg hauv daim siab los tsim ketone lub cev, muab lub zog ntxiv rau lub cev. Cov txiaj ntsig no tseem ceeb tshwj xeeb hauv cov xeev kev ntxhov siab xws li kev tshaib kev nqhis thiab yoo mov.

Cov lus qhia txog kev tswj hwm ntawm pancreatic islet muaj nuj nqi: Glucagon tuaj yeem tswj hwm insulin tso tawm ntawm pancreatic beta hlwb los ntawm kev ua haujlwm paracrine. Thaum cov ntshav qab zib nce ntxiv, glucagon secretion txo qis, txhawb kev tso tawm ntawm insulin ncaj qha;

Thaum cov piam thaj hauv ntshav txo qis, glucagon secretion nce ntxiv thaum inhibiting insulin secretion, tsim cov lus qhia tsis zoo ntawm "cov ntshav qabzib glucagon insulin" los tswj cov ntshav qab zib homeostasis.

Cov ntaub ntawv pov thawj:
1. Kev ua haujlwm ntawm lub cev ntawm glucagon thiab cov txheej txheem txawv txav hauv ntshav qab zib Suav Journal of Endocrinology thiab Metabolism, 2024
2. Glucagon secretion dysregulation nyob rau hauv hom 2 mob ntshav qab zib: Mechanisms thiab kho lub hom phiaj. Nature Reviews Endocrinology, 2025.
3. Cov yam ntxwv zais cia thiab qhov tseem ceeb ntawm cov tshuaj glucagon hauv cov neeg mob ntshav qab zib hom 2, suav nrog Journal of diabetes, 2024

Qhov saum npoo ntawm pancreatic alpha hlwb qhia tau hais tias GLP-1 receptor (GLP-1 R), uas belongs rau G protein coupled receptor (GPCR) B tsev neeg thiab yog 7-fold transmembrane glycoprotein. Nws extracellular domain yog ligand binding domain uas tuaj yeem paub txog GLP-1 thiab exenatide, uas yog lub hauv paus rauExenatide Txhajinhibit glucagon secretion.
Kev khi ntawm exenatide rau GLP-1 receptors hauv pancreatic alpha hlwb pom cov yam ntxwv hauv qab no:

1. High affinity thiab tshwj xeeb: Cov dissociation tas li (Kd) ntawm exenatide nrog GLP-1 receptor yog hais txog 0.3 nM, uas yog siab dua li ntawm natural GLP-1 (Kd yog hais txog 1.0 nM), thiab nws tsuas yog tshwj xeeb khi rau GLP-1 receptor, tsis muaj kev sib khi rau lwm yam cuam tshuam agon receptors xws li glucagon receptors.

2. Increased blood glucose dependent binding: When blood glucose levels rise (>3.9 mmol / L), qhov kev qhia ntawm GLP-1 receptors nyob rau saum npoo ntawm pancreatic alpha hlwb yog upregulated, thiab kev sib txuas ntawm exenatide thiab receptors yog ntxiv txhim kho, ua rau muaj kev cuam tshuam tseem ceeb ntawm glucagon secretion; Thaum cov ntshav qabzib zoo li qub lossis txo qis (<3.9 mmol/L), GLP-1 receptor expression is downregulated, and the binding of exenatide to the receptor is weakened, thereby reducing the inhibitory effect on glucagon secretion and preserving the compensatory secretion function of glucagon during hypoglycemia.

3. Persistence ntawm receptor activation: Exenatide, nyob rau hauv lub thib ob txoj hauj lwm, yog glycine (Gly) es tsis txhob ntawm lub ntuj GLP-1 alanine (Ala), uas muaj peev xwm tiv taus DPP-4 enzymatic degradation thiab muaj ib nrab-lub neej ncua mus rau 2.4 teev. Tom qab txhaj tshuaj subcutaneous, nws tuaj yeem txuas ntxiv siv nws cov txiaj ntsig hauv lub cev, txuas ntxiv ua haujlwm GLP-1 receptors thiab ua tiav qhov kev txwv ntev ntawm glucagon secretion.

Tom qab khi rau GLP-1 receptors, exenatide induces kev hloov hauv receptor conformation, activates downstream signaling pathways nyob rau hauv lub cell, thiab inhibits synthesis thiab secretion ntawm glucagon. Cov txheej txheem no ua raws li cov txheej txheem ntawm kev txiav txim ntawm ntuj GLP-1, tab sis vim muaj kev ruaj khov thiab ntev ntev ntawm kev txiav txim ntawm exenatide, cov nyhuv inhibitory tseem ceeb dua.

Core mechanism: Kev tswj ntawm intracellular signaling pathways (inhibition ntawm glucagon synthesis thiab secretion)

Txoj kev taw qhia ntawm glucagon secretion inhibits qhov txawv txav ntawm glucagon los ntawm ob theem "synthesis" thiab "secretion". Lub mechanism tshwj xeeb yog raws li nram no:

Ua kom lub Gs cAMP PKA teeb liab txoj hauv kev thiab inhibit glucagon secretion

Qhov no yog qhov tseem ceeb tshaj tawm txoj hauv kev los ntawm exenatide inhibits glucagon secretion, thiab cov txheej txheem tshwj xeeb yog raws li hauv qab no:
1. Kev khi ntawm exenatide rau GLP-1 receptors nyob rau saum npoo ntawm pancreatic alpha hlwb → receptor conformational hloov → ua kom intracellular Gs protein (alpha subunit dissociation);

2. Cov activated Gs protein alpha subunit khi thiab activates adenylate cyclase (AC) → AC catalyzes hloov ntawm ATP rau cyclic adenosine monophosphate (cAMP), nce intracellular cAMP concentration los ntawm 2-5 zaug;
3. cAMP khi thiab ua kom cov protein kinase A (PKA) → PKA catalyzes subunit dissociation thiab phosphorylation ntawm downstream phiaj proteins;

4. Phosphorylated lub hom phiaj cov protein tuaj yeem inhibit qhov tso tawm ntawm Ca ² ⁺ nyob rau hauv pancreatic alpha hlwb thiab suppress lub extracellular tso tawm ntawm glucagon granules, yog li ncaj qha txo qhov tso tawm ntawm glucagon.
Cov kev tshawb fawb tau pom tias exenatide tuaj yeem ua rau nce cAMP concentration hauv cov kab mob pancreatic islet hlwb ntawm cov neeg mob ntshav qab zib hom 2, txhim kho PKA kev ua, thiab txo cov glucagon tso tawm los ntawm 60% ~ 80% (tom qab noj mov), thiab cov nyhuv no yog nyob ntawm koob tshuaj - thaum koob tshuaj exenatide yog 10 agon μ glucagon inhibited ntau dua ib hnub, uas 5 μg ob zaug ib hnub.

Inhibit Ca ² ⁺ taw qhia txoj hauv kev thiab thaiv kev tso tawm ntawm glucagon granules

Ca ² ⁺ yog ib qho tseem ceeb taw qhia molecule rau lub extracellular tso tawm ntawm glucagon granules: nyob rau hauv ib txwm muaj xwm txheej, nce nyob rau hauv Ca ² ⁺ concentration nyob rau hauv pancreatic alpha hlwb ua rau lub fusion ntawm glucagon granules nrog lub cell membrane, ua tiav secretion. Exenatide inhibits Ca ² ⁺ taw qhia txoj hauv kev thiab thaiv glucagon secretion nyob rau hauv ob txoj kev:

Los ntawm Gs cAMP PKA kev taw qhia txoj hauv kev, phosphorylate Ca ² ⁺ channels, inhibit Ca ² ⁺ influx, thiab txo qis intracellular Ca ² ⁺ concentration;
2. Ua kom cov poov tshuaj raws (K ⁺ channels) kom ua rau cov kab mob pancreatic alpha cell ua kom muaj zog, ntxiv inhibit Ca ² ⁺ influx, thiab yog li thaiv qhov tso tawm ntawm glucagon granules.

Cov kev sim hauv vitro tau lees paub tias exenatide tuaj yeem txo qis intracellular Ca ² ⁺ concentration ntawm pancreatic alpha hlwb los ntawm 30% mus rau 40%, cuam tshuam qhov tso tawm ntawm glucagon, thiab cov nyhuv inhibitory no tuaj yeem thim rov qab los ntawm GLP-1 receptor antagonists (xws li Exendin-9-39), ua pov thawj tias nws cov nyhuv ntawm LP.

Cov ntaub ntawv pov thawj:
1. Molecular hauv paus ntawm exenatide-induced glucagon suppression nyob rau hauv hom 2 mob ntshav qab zib. Phau ntawv Journal of Biological Chemistry, 2024.
2. Kev tswj cov nyhuv thiab cov txheej txheem ntawm exenatide ntawm pancreatic alpha cell ua haujlwm Suav Pharmacological Bulletin, 2024
3. GLP-1 receptor agonists tswj glucagon secretion ntawm cAMP-PKA txoj kev taw qhia. Mob ntshav qab zib, 2024.
4. FDA. Byetta (Exenatide Txhaj) Phau Ntawv Teev Npe (2024 Edition)

Cim npe nrov: exenatide txhaj tshuaj, lwm tus neeg, manufacturers, hoobkas, lag luam wholesale, yuav, nqe, tej, kev muag khoom