Shaanxi BLOOM Tech Co., Ltd. yog ib qho ntawm cov tuam ntxhab thiab cov muag khoom ntawm argipressin acetate hauv Suav teb. Txais tos rau cov lag luam wholesale bulk zoo argipressin acetate muag ntawm no los ntawm peb lub hoobkas. Kev pabcuam zoo thiab tus nqi tsim nyog muaj.
Argipressin acetate hmoovyog ib qho kev sib xyaw ua ke cyclic nonapeptide hormone uas simulates qhov kev txiav txim ntawm natural antidiuretic hormone (AVP), exerting dual physiological zog ntawm vasoconstriction thiab antidiuretic. Nws cov qauv tshuaj muaj cuaj amino acids, tsim cov qauv cyclic los ntawm disulfide bonds ntawm cysteine residues ntawm txoj haujlwm 1 thiab 6. Nws muaj cov amino acids uas muaj ntxhiab xws li tyrosine thiab phenylalanine, nrog rau cov mis molecular ntawm C48H69N15O14S2 thiab molecular hnyav ntawm kwv yees li 28.44.
Cov tshuaj ua tiav nws txoj haujlwm los ntawm kev ua kom lub V1a receptor hauv vascular du leeg thiab V2 receptor hauv lub raum tubules
Vasoconstriction nyhuv:
Tom qab khi rau V1a receptors, phospholipase C (PLC) - inositol triphosphate (IP3) - calcium ion (Ca ² ⁺) qhia txoj hauv kev tau qhib, ua rau cov leeg nqaij du thiab nce peripheral vascular tsis kam, yog li nce ntshav siab. Cov txheej txheem no feem ntau siv los tswj cov ntshav vasodilatory mob xws li esophageal variceal rupture los ntshav.
Antidiuretic nyhuv:
Ua kom cov adenylate cyclase (AC) - cyclic adenosine monophosphate (cAMP) - protein kinase A (PKA) txoj hauv kev los ntawm V2 receptor txhawb cov membrane insertion ntawm aquaporin 2 (AQP2) nyob rau hauv lub raum khaws cov duct, txhim kho cov dej reabsorption, txo cov tsos mob ntawm cov zis hauv nruab nrab.
Peb cov khoom
Argipressin Acetate COA
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| Certificate of Analysis | ||
| Compound npe | Argipressin Acetate | |
| Qib | Pharmaceutical qib | |
| CAS Nr. | 129979-57-3 | |
| Ntau | 60g | |
| Ntim txheem | PE hnab + Al foil hnab | |
| Chaw tsim tshuaj paus | Shaanxi BLOOM TECH Co., Ltd | |
| Ntau No. | 202501090069 | |
| MFG | Peb 9, 2025 | |
| EXP | Peb 8, 2028 | |
| Qauv |
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| 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% | 0.54% |
| Poob rau ziab | Tsawg dua lossis sib npaug li 1.0% | 0.42% |
| 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% | 99.98% |
| Ib leeg impurity | <0.8% | 0.52% |
| Tag nrho microbial suav | Tsawg dua lossis sib npaug li 750cfu / g | 95 |
| 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 | 500ppm ua |
| Cia | Khaws rau hauv qhov chaw kaw, tsaus, thiab qhuav hauv qab -20 degree | |
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| Chemical Formula: | C46H65N15O12S2 |
| Exact Mass: | 1083 |
| Molecular Luj: | 1084 |
| m/z: | 1083 (100.0%), 1084 (49.8%), 1085 (12.1%), 1085 (9.0%), 1084 (5.5%), 1086 (4.5%), 1085 (2.8%), 1085 (2.5%), 1086 (1.9%), 1086 (1.2%), 1087 (1.1%) |
| Elemental Analysis: | C, 50.96; H, 6.04; N, 19.38; O, 17.71; S, 5.91 |
Argipressin acetate hmoov, tseem hu ua antidiuretic hormone (ADH), yog cuaj peptide hormone synthesized los ntawm neurons hauv hypothalamic supraoptic thiab paraventricular nuclei. Nws tso tawm rau hauv cov hlab ntsha los ntawm lub caj pas pituitary thiab ua lub luag haujlwm tseem ceeb hauv kev tswj cov kua dej sib npaug, ntshav siab homeostasis, thiab kev ntxhov siab. Nws txoj haujlwm physiological tau ua tiav los ntawm kev khi tshwj xeeb rau cov tswv cuab ntawm G protein ua ke receptor (GPCR) tsev neeg, nrog rau lub ntsiab receptor subtypes suav nrog V1a, V1b, thiab V2 receptors.
Receptor faib thiab kev ua haujlwm tshwj xeeb
Kev faib tawm ntawm vasopressin TFA receptor subtypes hauv cov ntaub so ntswg yog kev xaiv heev, txiav txim siab lawv cov kev ua haujlwm sib txawv.
V1a receptor (vasopressin hom 1a receptor)
Kev faib tawm: dav dav hauv vascular du leeg, myocardial cells, daim siab hlwb, platelets, thiab hauv nruab nrab paj hlwb (xws li hippocampus thiab amygdala).
Muaj nuj nqi:
Vasoconstriction: Nyob rau hauv vascular du nqaij, vasopressin TFA khi rau V1a receptors thiab ua kom cov phospholipase C (PLC) - inositol triphosphate (IP3) - calcium ion (Ca ² ⁺) taw qhia txoj hauv kev, ua rau muaj kev nce hauv intracellular Ca ⁺ kev cog lus ntawm cov leeg nqaij, ² ua kom cov leeg nqaij du, ² nce ntxiv hauv cov leeg nqaij. vascular tsis kam, thiab yog li nce ntshav siab. Cov txheej txheem no yog qhov tseem ceeb tshwj xeeb tshaj yog thaum cov ntshav ntim tsis txaus (xws li los ntshav lossis lub cev qhuav dej), vim nws tuaj yeem tswj cov hlab ntshav ruaj khov.
Cardiac hypertrophy: Ua kom muaj V1a receptors hauv cov hlwb myocardial tuaj yeem txhawb nqa cov protein synthesis thiab cell proliferation. Lub sij hawm ntev stimulation ntau dhau tuaj yeem ua rau pathological cardiac hypertrophy, uas cuam tshuam nrog kev loj hlob ntawm lub plawv tsis ua haujlwm.
Platelet aggregation: AVP txhim kho platelet aggregation muaj peev xwm los ntawm V1a receptors thiab koom nrog cov txheej txheem ntawm thrombosis.
Kev tswj hwm hauv nruab nrab: Hauv cov cheeb tsam hauv hlwb xws li hippocampus thiab amygdala, V1a receptors koom nrog hauv kev kawm thiab kev nco, kev tswj kev xav, thiab kev tswj hwm kev coj noj coj ua.
V1b receptor (vasopressin type 1b receptor)
Kev faib tawm: Feem ntau faib rau hauv cov qog pituitary anterior, pancreatic alpha / beta hlwb, lub raum khaws cov ducts, thiab hauv nruab nrab lub paj hlwb (xws li hypothalamus thiab prefrontal cortex).
Muaj nuj nqi:
Tso tawm ntawm adrenocorticotropic hormone (ACTH): Nyob rau hauv lub anterior pituitary caj pas, vasopressin TFA khi rau V1b receptors thiab activates PLC -IP3-Ca ² ⁺ txoj hauv kev los txhawb ACTH secretion, uas nyob rau hauv lem activates adrenal cortex mus rau secrete cortisol cores ntawm kev nyuaj siab, pituitary adrenal axis (HPA axis).
Glucagon secretion: Ua kom muaj V1b receptors hauv pancreatic alpha hlwb tuaj yeem txhawb nqa glucagon tso tawm thiab koom nrog kev tswj ntshav qabzib.
Kev xav thiab kev coj tus cwj pwm: Kev qhia ntawm V1b receptors nyob rau hauv lub hauv paus paj hlwb muaj feem xyuam rau lawv cov kev tswj lub luag hauj lwm nyob rau hauv kev ntxhov siab vim, kev nyuaj siab, thiab aggressive cwj pwm. Piv txwv li, nyob rau hauv cov neeg mob uas muaj kev nyuaj siab loj heev, upregulation ntawm V1b receptor qhia nyob rau hauv lub pituitary caj pas ua rau kom ntau dhau ntawm HPA axis, exacerbating cov tsos mob ntawm tsis zoo mus ob peb vas.
V2 receptor (vasopressin type 2 receptor)
Kev faib tawm: Qhia tshwj xeeb hauv lub raum khaws cov duct lub ntsiab hlwb thiab lub raum lub raum tubular epithelial hlwb.
Muaj nuj nqi:
Antidiuretic nyhuv: AVP khi rau V2 receptor thiab ua kom lub adenylate cyclase (AC) - cyclic adenosine monophosphate (cAMP) - protein kinase A (PKA) taw qhia txoj hauv kev, txhawb nqa kev thauj ntawm aquaporin 2 (AQP2) los ntawm intracellular luminous peripheral vesicles, nce mus rau hauv cov ntaub so ntswg. dej reabsorption, txo cov zis tso zis, thiab tswj cov kua osmotic siab tshuav.
Kev tswj hwm ntawm aquaporins: Lub V2 receptor signaling txoj kev tseem koom nrog kev hloov kho phosphorylation ntawm AQP2 thiab kev saib xyuas ntawm daim nyias nyias. Lub sij hawm ntev vasopressin TFA stimulation tuaj yeem txhim kho AQP2 kev qhia thiab txhim kho lub raum lub peev xwm los rov nqus dej.
Core teeb liab txoj kev tsom xam
AVP receptors qhib cov kev taw qhia downstream los ntawm kev sib txawv G protein coupling mechanisms, ua tiav cov haujlwm tshwj xeeb:
V1a/V1b receptor signaling pathway (PLC-IP3-Ca ² ⁺ txoj hauv kev)
Mechanism: Vasopressin TFA khi rau V1a / V1b receptors, ua kom Gq protein thiab tom qab ua kom PLC. PLC catalyzes hydrolysis ntawm phosphatidylinositol 4,5-diphosphate (PIP2) los tsim IP3 thiab diacylglycerol (DAG). IP3 khi rau IP3 receptor ntawm endoplasmic reticulum, tso cia Ca ² ⁺ mus rau hauv cytoplasm thiab ua rau muaj kev nce hauv intracellular Ca ² ⁺ concentration; DAG activates protein kinase C (PKC) thiab koom nrog kev tswj hwm ntawm cell proliferation thiab sib txawv.
Physiological teebmeem:
Vascular smooth nqaij contraction (V1a receptor).
ACTH secretion (V1b receptor).
Platelet aggregation (V1a receptor).
V2 receptor signaling pathway (AC cAMP PKA txoj hauv kev)
Mechanism: Tom qab vasopressin TFA khi rau V2 receptor, nws activates Gs protein, uas nyob rau hauv lem activates AC. AC catalyzes ATP los tsim cAMP, uas ua raws li tus xa xov thib ob los qhib PKA. PKA phosphorylates lub hom phiaj cov protein (xws li AQP2), txhawb nqa lawv cov membrane thauj thiab ua kom ua haujlwm.
Physiological teebmeem:
AQP2 membrane insertion txhim khu lub raum dej reabsorption (V2 receptor).
Lub sij hawm ntev stimulation tuaj yeem txhim kho AQP2 noob qhia thiab nce aquaporin synthesis.
Hla kev cai thiab kev koom ua ke
Cov nyhuv synergistic ntawm Ca ² ⁺ thiab cAMP: Hauv lub raum khaws cov duct hlwb, V2 receptor signaling txoj kev tuaj yeem qhib Rap1 GTPase los ntawm Epac (hloov cov protein ncaj qha ua rau cAMP) txoj hauv kev, txhawb nqa AQP2 membrane insertion. Nyob rau tib lub sijhawm, Ca ² ⁺ kev taw qhia tuaj yeem txhim kho PKA kev ua haujlwm los ntawm kev ua kom muaj zog (CaM), ua kom muaj kev sib koom ua ke.
Receptor desensitization thiab internalization: Lub sij hawm ntev vasopressin TFA stimulation tuaj yeem ua rau receptor phosphorylation (xws li - inhibitory protein mediated), ua rau receptor internalization, txo cov cell rhiab heev rauargipressin acetate hmoov, thiab tsim ib qho kev tawm tswv yim tsis zoo rau kev tswj hwm txoj cai.
Pathophysiological tseem ceeb thiab kev siv tshuaj kho mob
Qhov txawv txav ntawm vasopressin TFA receptor signaling pathway yog ze ze rau ntau yam kab mob, thiab cov tswv yim kev cuam tshuam rau cov receptors tau dhau los ua lub ntsiab lus kub hauv kev kho mob:
Lub plawv tsis ua hauj lwm
Mechanism: Nyob rau hauv lub plawv tsis ua hauj lwm, txo cov ntshav ntim thiab txo lub raum perfusion siab tshaj activate vasopressin TFA secretion los ntawm tsis osmotic siab stimulation (xws li atrial baroreceptors), ua rau V1a receptor mediated vasoconstriction thiab V2 receptor mediated water retention, aggravating pulmonary congestion thiab hyponatremia.
Kev kho: V2 receptor antagonists (xws li Tovaptan) tuaj yeem txo cov dej rov qab los ntawm kev thaiv AVP-V2 receptor khi, txhim kho hyponatremia thiab kua dej tuav, thiab tsis txhob qhib lub renin angiotensin aldosterone system (RAAS) kom tsis txhob muaj kev pheej hmoo ntawm electrolyte tsis meej ntawm cov tshuaj diuretics.
Hyponatremia
Mechanism: Nyob rau hauv lub syndrome ntawm txawv txav antidiuretic hormone secretion (SIADH), ntau vasopressin TFA secretion ua rau dej tuav thiab diluted hyponatremia.
Kev Kho Mob: V2 receptor antagonists tuaj yeem txhawb nqa cov dej tso tawm dawb, kho hyponatremia, thiab zam kev txo cov ntshav ntim ntau dhau los ntawm diuresis ntau dhau.
Kev ntxhov siab thiab kev nyuaj siab
Mechanism: V1b receptors ua lub luag haujlwm tseem ceeb hauv kev ua haujlwm dhau ntawm HPA axis, thiab lawv cov kev tswj hwm tau cuam tshuam nrog cov tsos mob kev nyuaj siab.
Kev Kho Mob: Xaiv V1b receptor antagonists (xws li SSR149415) inhibit ACTH secretion, txo cov qib cortisol, txo kev ntxhov siab thiab kev nyuaj siab, thiab tam sim no nyob rau hauv kev sim tshuaj.
Ntshav siab
Mechanism: V1a receptor mediated vasoconstriction yog ib qho ntawm cov txheej txheem tseem ceeb ntawm kev kub siab, tshwj xeeb tshaj yog nyob rau hauv ntsev rhiab siab qhov twgargipressin acetate hmoovrhiab heev.
Kev Kho Mob: V1a receptor antagonists tuaj yeem txo cov hlab ntsha peripheral, tab sis lawv cov kev mob tshwm sim ntawm myocardial contractility thiab platelet muaj nuj nqi yuav tsum sib npaug.
Arginine vasopressin ua tiav ntau yam kev ua haujlwm ntawm lub cev xws li vasoconstriction, dej reabsorption, kev ntxhov siab, thiab kev tswj kev xav los ntawm PLC-IP3-Ca ²⁺ thiab AC cAMP PKA kev taw qhia txoj hauv kev ntawm V1a, V1b, thiab V2 receptor subtypes. Qhov txawv txav ntawm nws txoj kev taw qhia yog ze ze rau cov kab mob xws li lub plawv tsis ua hauj lwm, hyponatremia, ntxhov siab vim, thiab kev nyuaj siab. Cov tswv yim xaiv kev cuam tshuam rau lub hom phiaj receptors, xws li V2 receptor antagonists thiab V1b receptor antagonists, muab cov lus qhia tshiab rau kev kho mob. Cov kev tshawb fawb yav tom ntej yuav tsum tau qhia ntxiv txog cov kev tswj hwm kev tswj hwm ntawm cov receptor subtypes hauv cov kab mob nyuaj, txhim kho cov txiaj ntsig zoo thiab tsis tshua muaj kev phiv tshuaj, thiab tshawb nrhiav cov txiaj ntsig kho mob ntawm vasopressin TFA teeb liab txoj hauv kev hauv nruab nrab paj hlwb kab mob.
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