Angiotensin Acetate, Suav tus qauv lub npe yog angiotensin II acetate, tseem hu ua angiotensin II acetate, (Val5) - angiotensin II, los yog vasopressin. Nws yog acetate daim ntawv ntawm angiotensin II (Ang II), lub ntsiab active peptide nyob rau hauv lub renin -angiotensin system (RAS). Nws yog ib qho khoom siv hluavtaws octapeptide cov tshuaj hormones uas sib xyaw ua ke muaj zog vasoconstrictive kev ua ub no, kev tswj hwm endocrine, thiab kev tswj cov teeb liab ntawm lub plawv. Nws qhov chaw tseem ceeb yog qhov tseem ceeb ntawm RAS system, tus neeg nruab nrab ntawm kev tswj ntshav siab, thiab cov cuab yeej kub rau kev tshawb fawb kab mob plawv. Nws muaj txiaj ntsig tsis tuaj yeem hloov pauv hauv kev tshawb fawb physiological thiab pathological, kab mob qauv kev tsim kho, kev tsim tshuaj, thiab kev kho mob xwm txheej ceev.
Peb cov khoom Description
Angiotensin AcetateCOA
 |
||
| Certificate of Analysis | ||
| Compound npe | Cov tshuaj Angiotensin acetate | |
| Qib | Pharmaceutical qib | |
| CAS Nr. | 58-49-1 | |
| Ntau | 50g | |
| Ntim txheem | PE hnab + Al foil hnab | |
| Chaw tsim tshuaj paus | Shaanxi BLOOM TECH Co., Ltd | |
| Ntau No. | 202601090069 | |
| 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% | 0.57% |
| Poob rau ziab | Tsawg dua lossis sib npaug li 1.0% | 0.46% |
| 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% | 0.56% |
| Tag nrho microbial suav | Tsawg dua lossis sib npaug li 750cfu / g | 150 |
| 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 -20 degree | |
|
|
||
|
|
||
| Tshuaj Formula: | C49H69N13O12 |
| Exact Mass: | 1031.52 |
| Molecular Luj: | 1032.17 |
| m/z: | 1031.52 (100.0%), 1032.52 (53.0%), 1033.53 (13.8%), 1032.52 (4.8%), 1033.52 (2.5%), 1033.52 (2.5%), 1034.53 (2.3%), 1034.53 (1.3%) |
| Elemental Analysis: | C, 57.02; H, 6.74; N, 17.64; O, 18.60 |
Raws li kev npaj ruaj khov ntawm cov tub ntxhais davhlau ya nyob twg active peptide ntawm renin angiotensin aldosterone system (RAAS),Cov tshuaj angiotensin acetateTsis tsuas yog koom nrog kev tswj hwm ntshav siab thiab dej ntsev sib npaug, tab sis tseem tswj hwm kev ua haujlwm ntawm cov pob txha, calcium thiab phosphorus metabolism, PTH secretion, vitamin D activation, thiab pob txha lub raum axis cuam tshuam los ntawm AT1 / AT2 receptor- kho kom haum xeeb-channel signaling network.Renal Osteodystrophy feem ntau cov kab mob metabolic (ROD) Cov theem kawg ntawm cov kab mob raum ntev (CKD), tus cwj pwm los ntawm calcium thiab phosphorus metabolism tsis zoo, vitamin D ua kom tsis zoo, theem nrab hyperparathyroidism (SHPT), pob txha tsim / resorption imbalance, thiab pathological hloov kho ntawm cov pob txha raum axis, cuam tshuam rau lub neej zoo thiab kev ciaj sia ntawm cov neeg mob.
Lub raum osteodystrophy thiab pathological hloov kho ntawm cov pob txha raum axis
Clinical Status and Hazards of Renal Osteodystrophy (ROD)
Lub raum osteodystrophy (ROD) yog lub cev pob txha tshwm sim ntawm cov kab mob hauv lub raum tsis zoo thiab cov kab mob pob txha (CKD-MBD), txhais tau tias yog ib qho mob ntawm cov pob txha txawv txav, cov ntxhia hauv tsev, thiab vascular calcification hauv cov neeg mob CKD tshwm sim los ntawm kev poob qis hauv lub raum ua haujlwm. Cov ntaub ntawv kho mob qhia tau hais tias ntau dua 80% ntawm CKD theem 5 (kev lim ntshav) cov neeg mob muaj qhov sib txawv ntawm ROD, nrog rau 40% ntawm cov neeg mob ntshav lim ntshav tau ntsib cov mob pob txha loj tom qab ib xyoos, pom tias mob pob txha, pob txha, pob txha deformities, luv luv qhov siab, thiab muaj kev pheej hmoo ntau ntxiv ntawm cov hlab plawv tsis ua haujlwm, calification.
Cov yam ntxwv tseem ceeb ntawm ROD muaj xws li:
Kev cuam tshuam ntawm calcium thiab phosphorus metabolism: hyperphosphatemia, hypocalcemia, thiab nce calcium phosphorus khoom;
Cov metabolism hauv cov vitamin D tsis zoo: txo qis kev ua haujlwm ntawm lub raum 1 - hydroxylase thiab tsis txaus synthesis ntawm cov vitamin D3 (1,25- (OH) ₂ D3);
Secondary hyperparathyroidism (SHPT): kev tso tawm ntau dhau ntawm PTH drives txhim kho pob txha resorption;
Kev tsis sib haum xeeb hauv kev kho pob txha: txo qis kev ua haujlwm ntawm osteoblast, overactivation ntawm osteoclasts, txo cov pob txha loj, thiab kev puas tsuaj ntawm pob txha microstructure;
Pathological remodeling ntawm pob txha raum axis: raum raug mob thiab txawv txav cov pob txha metabolism tsav ib leeg, tsim ib tug vicious voj voog.
Physiological kev sib cuam tshuam thiab pathological remodeling mechanism ntawm pob txha raum axis
Pob txha raum Axis yog ib qho kev sib txuas endocrine uas txuas cov pob txha thiab ob lub raum. Nyob rau hauv physiological tej yam kev mob, nws tswj cov pob txha raum homeostasis los ntawm calcium thiab phosphorus metabolism, vitamin D activation, PTH kev cai, thiab pob txha derived yam tseem ceeb (osteocalcin, FGF23).
Cov kev cai zoo ntawm cov pob txha raum axis nyob rau hauv physiological mob
Lub raum → Pob txha: Raum 1 - hydroxylase converts 25- (OH) D rau 1,25- (OH) ₂ D3, txhawb txoj hnyuv calcium nqus, osteoblast txawv, thiab pob txha matrix mineralization; Lub raum tso tawm phosphorus thiab khaws cov calcium, tswj qhov sib npaug ntawm cov ntshav calcium thiab phosphorus, thiab inhibit PTH ntau dhau.
Pob txha → ob lub raum: Osteoblasts secrete osteocalcin (OC), uas tswj lub raum insulin rhiab heev thiab calcium reabsorption; Osteocytes secrete fibroblast kev loj hlob yam tseem ceeb 23 (FGF23), uas inhibits lub raum 1 - hydroxylase kev ua si, txhawb phosphorus excretion, thiab ua raws li cov lus qhia tsis zoo.
Lub voj voog vicious ntawm pob txha raum axis nyob rau hauv cov kab mob pathological (ROD core mechanism)
Kev loj hlob ntawm CKD ua rau tsis muaj kev puas tsuaj rau lub raum kev ua haujlwm, ua rau muaj kev hloov pauv ntawm cov pob txha raum axis, ua rau lub cev tsis zoo ntawm lub raum raug mob → pob txha metabolism tsis zoo → ua rau lub raum raug mob:
Txo lub raum ua haujlwm → phosphorus excretion disorder → hyperphosphatemia: hyperphosphatemia ncaj qha inhibits 1 - hydroxylase, txo 1,25- (OH) ₂ D3, thiab induces vascular calcification;
Tsawg 1,25- (OH) ₂ D3 → txo cov plab hnyuv calcium nqus → hypocalcemia → PTH secretion ntau dhau (SHPT);
Siab PTH → ua kom osteoclasts → txhim kho pob txha resorption → tso tawm cov pob txha calcium → ncua sij hawm nce ntawm cov ntshav calcium → aggravation ntawm lub raum calcium deposition;
Txhim kho pob txha resorption → txo cov pob txha loj, kev puas tsuaj ntawm pob txha microstructure → kev loj hlob ntawm ROD;
Siab phosphorus, siab PTH, qis 1,25- (OH) ₂ D3 → Ua kom tso tawm ntawm FGF23 los ntawm cov pob txha hlwb → Ntxiv inhibition ntawm 1 - hydroxylase → aggravation ntawm vitamin D deficiency.
Cov txheej txheem tseem ceeb ntawm kev txhim kho pathological ntawm cov pob txha raum axis
Kev lig kev cai, nws ntseeg tau tias RAAS tsuas yog tswj cov ntshav siab thiab dej ntsev sib npaug. Txawm li cas los xij, cov kev tshawb fawb tsis ntev los no tau lees paub tias RAAS (tshwj xeeb yog Ang II) yog qhov tseem ceeb ntawm kev sib cuam tshuam hauv cov pob txha raum axis, qhia hauv zos hauv ob lub raum thiab pob txha. Nws ncaj qha tswj cov pob txha ua haujlwm, calcium thiab phosphorus metabolism, PTH secretion, thiab vitamin D ua kom dhau los ntawm AT1 / AT2 receptors.
Raws li qhov siab -purity, ruaj khov, thiab dej siab heev- soluble exogenous Ang II npaj,Cov tshuaj angiotensin acetateyog lub cuab yeej tseem ceeb rau kev kawm lub luag haujlwm ntawm Ang II hauv cov pob txha raum axis thiab muab cov phiaj xwm muaj peev xwm rau ROD cov phiaj xwm kev cuam tshuam. Nws lub luag haujlwm hauv ROD yog concentration nyob, receptor subtype dependent, thiab microenvironment dependent:
High concentration (pathological qib, 10 ⁻⁸ ~ 10 ⁻⁶ mol / L): activates AT1 receptors, drives pob txha resorption, inhibits pob txha tsim, exacerbates calcium phosphate mob, txhawb vascular calcification, thiab accelerates kev loj hlob ntawm ROD;
Tsawg concentration (physiological / reparative qib, 10 ⁻¹² ~ 10 ⁻¹⁰ mol / L): activates AT2 / Mas receptors, txhawb cov pob txha tsim, inhibits pob txha resorption, txhim kho calcium thiab phosphorus metabolism, txo vascular calcification, thiab exerts pob txha tiv thaiv.
Cov ntaub ntawv siv tau
- KDIGO. 2024. Cov Lus Qhia Txog Kev Kho Mob rau Kev Ntsuam Xyuas thiab Kev Tswj Xyuas Kab Mob Raum Ntev -Mineral Bone Disorder
- Tuam Tshoj Medical Association Nephrology ceg ob txhiab thiab nees nkaum- plaub tus kws tshaj lij pom zoo rau kev kuaj mob thiab kev kho mob raum osteodystrophy
- PMC. 2025. Pob txha-Kidney Axis: Tus Txheej Txheem Tseem Ceeb ntawm Mineral Homeostasis hauv Kab Mob Raum Ntev
- PubMed. 2025. Angiotensin II: Tus Txheej Txheem Novel ntawm Pob Txha Metabolism hauv Raum Osteodystrophy
- TargetMol. 2026. Angiotensin II human acetate Cov Ntaub Ntawv Cov Khoom Siv thiab Kev Ua Txhaum Cai
Lub zog physicochemical thiab kev faib tawm ntawm cov pob txha raum axis ntawm cov khoom no
Receptor binding yam ntxwv (bidirectional tswj hauv paus)
Ang II Acetate ua los ntawm AT1 receptor (AT1R), AT2 receptor (AT2R), thiab Mas receptor (MasR), nrog rau kev sib txawv thiab kev ua haujlwm antagonism ntawm peb qhov loj receptors hauv pob txha raum axis
AT1R: Tshaj tawm ntau hauv ob lub raum (tubules, mesangial cells, thiab periglomerular cells), pob txha (osteoclasts, osteoblasts, osteoblasts, chondrocytes), thiab cov qog parathyroid. High concentrations ntawm Ang II nyiam khi (KD=1-5 nM), kho cov kab mob kev puas tsuaj;
AT2R: Tsis tshua muaj kev qhia hauv ob lub raum (cov hlwb interstitial, endothelial hlwb), pob txha (osteoblasts, pob txha hlwb, pob txha pob txha mesenchymal qia hlwb), cov qog parathyroid, upregulated 5-10 zaug tom qab raug mob, tsawg concentration Ang II nyiam khi (KD=50-100nM), kho kho thiab tiv thaiv;
MasR: co qhia nrog AT2R nyob rau hauv ob lub raum, pob txha, thiab vascular endothelium, tshwj xeeb khi rau Ang 1-7 (Ang II degradation khoom) thiab synergistically amplifying lub kho nyhuv nrog AT2R.
Local RAAS system
Lub raum yog lub luag haujlwm tseem ceeb ua haujlwm los ntawm RAAS, thiab thaum lub sijhawm CKD, RAAS hauv zos hauv lub raum yog overactivated, ua rau muaj kev nce ntxiv hauv Ang II concentration.
Generating site: Perispherical cells secrete renin → angiotensinogen hloov mus rau Ang I → ACE catalyzes tiam ntawm Ang II; Lub raum tubular epithelial hlwb, mesangial hlwb, thiab endothelial hlwb autocrine/paracrine Ang II;
Kev faib tawm cov yam ntxwv: Tom qab kev txhaj tshuaj ntawm Ang II Acetate, nws zoo dua khaws cia hauv lub raum cortex (lub raum tubules, glomeruli), nrog rau cov concentration 2-3 zaug ntawm cov ntshav, ncaj qha tswj lub raum calcium thiab phosphorus metabolism, 1 - hydroxylase kev ua, thiab PTH rhiab heev.
Local RAAS system ntawm cov pob txha (kev tswj ncaj qha ntawm cov pob txha metabolism)
Muaj cov kab ke RAAS ua tiav hauv zos hauv cov pob txha pob txha, qhov twg osteoblasts, osteoclasts, pob txha hlwb, thiab cov pob txha pob txha mesenchymal qia hlwb tuaj yeem ua rau tag nrho cov synthesize thiab secrete Ang II thiab nws cov receptors, ntawm nws tus kheej tswj cov pob txha metabolism los ntawm circulating RAAS.
Osteoblasts: siab qhia ntawm AT1R / AT2R, synthesis ntawm Ang II, kev tswj ntawm kev loj hlob, sib txawv, thiab cov pob txha matrix synthesis;
Osteoclasts: siab qhia ntawm AT1R, qis qhia ntawm AT2R, Ang II txhawb kev sib txawv, ua kom, thiab pob txha resorption los ntawm AT1R;
Cov pob txha pob txha: cov pob txha ntau tshaj plaws, qhia AT1R / AT2R, zais RANKL thiab FGF23, tswj cov pob txha hloov kho thiab calcium phosphate metabolism;
Cov pob txha pob txha- muab tau los ntawm mesenchymal qia hlwb (MSCs) nthuav qhia AT2R, thiab qis qis ntawm Ang II txhawb kev sib txawv osteogenic thaum inhibiting adipogenic sib txawv.
Lub caj pas parathyroid qhia AT1R / AT2R, thiab Ang II ncaj qha tswj PTH synthesis thiab tso tawm:
Kev ua kom AT1R: txhawb nqa PTH gene transcription, synthesis, thiab tso tawm, exacerbates SHPT;
Kev ua kom AT2R: inhibits PTH secretion thiab txhim kho SHPT.
Cov ntaub ntawv siv tau
- TargetMol. 2026. Angiotensin II human acetate Pharmacological Properties thiab Receptor Binding
- PMC. 2025. Hauv zos Renin-Angiotensin System hauv pob txha: Tus Txheej Txheem Tseem Ceeb ntawm Pob Txha Metabolism
- PubMed. 2025. Angiotensin II Receptor Expression nyob rau hauv lub raum thiab pob txha thaum mob raum mob
- EMA. 2019. Angiotensin II Acetate Summary of Product Yam ntxwv
- Suav Phau ntawv Journal ntawm Pharmacology thiab Toxicology ob txhiab thiab kaum rau Kev tshawb fawb kev nce qib ntawm cov txheej txheem thiab kev kho lub hom phiaj ntawm renin-angiotensin system hauv osteoporosis
Cov lus nug nquag
Puas yog soluble hauv PBS (pH 7.2) lossis tsis?
+
-
Txawm hais tias qhov no yog cov ntaub ntawv solubility, hauv cov ntawv thov, ntau tus kws tshawb fawb yuav sim npaj cov kev daws teeb meem ntau dua (xws li 5 lossis 10 mg / mL). Thaum cov concentration ntau tshaj 1 mg / mL, cov tshuaj yuav tsis tuaj yeem ua turbid tam sim ntawd, tab sis thaum lub sij hawm txias los yog khov, cov peptide ntu yuav maj mam los nag, uas ua rau cov concentrations qis dua cov nqi suav. Acetate angiotensin muaj cov nqi txo qis thiab txhim kho kev sib cuam tshuam hydrophobic ntawm cov molecules nyob rau hauv ib puag ncig nruab nrab ze rau lub cev pH. Nws yog ib qho yooj yim los tsim cov aggregates lossis precipitates, uas yog ib qho kev coj cwj pwm ntawm ntau qhov nruab nrab ntev hydrophobic peptides hauv nruab nrab tsis muaj kev daws teeb meem.
YogCov tshuaj angiotensin acetatethiab angiotensin hydrochloride ua tib yam hauv vivo?
+
-
Ob qho tib si theoretically sib npaug hauv cov tshuaj pharmacological, tab sis muaj qhov sib txawv ntawm solubility, hygroscopicity, thiab formulation compatibility. Acetic acid yog cov kua qaub uas tsis muaj zog (pKa 4.76), muaj zog heev, thiab yooj yim tshem tawm los ntawm khov- ziab; Hydrochloric acid yog cov kua qaub uas muaj zog, tsim cov ntawv ntsev uas ruaj khov dua tab sis yuav muaj qhov sib txawv hygroscopicity. Acetate angiotensin yog ib daim ntawv ntsev ntau dua hauv kev kawm thiab kev lag luam tshuaj, vim nws yooj yim dua los npaj rau hauv cov hmoov fluffy los ntawm khov - ziab.
Qhov "pom meej" angiotensin cov ntsiab lus ntawm ob daim ntawv ntsev sib txawv (vim qhov sib txawv molecular hnyav ntawm counterions). Hauv cov kev tshawb fawb uas xav tau cov koob tshuaj meej heev (xws li micro twj tso kua mis infusion), kev suav yuav tsum yog raws li cov ntsiab lus tseeb ntawm peptide feem (tsis yog qhov hnyav tag nrho ntawm daim ntawv ntsev).
Cim npe nrov: angiotensin acetate, Tuam Tshoj angiotensin acetate manufacturers, lwm tus neeg
