Semax Peptide

Semax peptideyog ib qho hluavtaws heptapeptide muab tau los ntawm ACTH (4-10) fragment ntawm adrenocorticotropic hormone (ACTH) thiab tau pom zoo nyob rau hauv Russia thiab lwm lub teb chaws rau kev kho mob adjuvant nyob rau theem mob stroke thiab kev txawj ntse. Nws cov yam ntxwv tseem ceeb yog kev txhim kho ntawm neurotrophic thiab tiv thaiv -txoj kev mob / tshuaj tiv thaiv kab mob los ntawm melanocortin receptor axis (tsuas yog MC4R), qhia txog kev tiv thaiv neuroprotective thiab pro-plasticity cuam tshuam hauv tsiaj thiab kev tshawb fawb thaum ntxov.

Shaanxi Medibridge muab 99.5% purity Semax hmoov rau kev tshawb fawb txiav. Ua raws li QC nruj nrog HPLC/MS pov thawj, peb RUO-qib Semax (MEHFPGP) muab kev ua tau zoo ib yam, zoo heev solubility, thiab txhim khu kev qha batch-rau-batch reproducibility. Customize labeling thiab formulation ntawm kev thov. Xaiv Medibridge rau kev ntseeg siab zoo, kev pabcuam teb, thiab cov txiaj ntsig tau txais txiaj ntsig hauv kev tshawb fawb neuroprotection thiab neuroplasticity.

Peb qhov zoo

1. Purity: HPLC Ntau dua lossis sib npaug li 99.5%; kev lees paub los ntawm LC-MS/MS; puv COA

2. Tsawg endotoxin thiab qis-TFA/acetate ntsev xaiv

3. Optimized lyophilization: sai dissolution, tsawg adsorption

4. Tight batch sib xws nrog kev tso tawm specs thiab cov qauv khaws cia

5. Customization: pob qhov ntau thiab tsawg, daim ntawv lo, amidation, fluorescent / biotin cim npe

6. Kev them nyiaj yug daim ntawv thov: MC4R-cAMP/ERK-BDNF axis raws tu qauv ntawm kev thov

Mechanism ntawm Action

Luv luv:Semaxpeptideyog ib qho ACTH fragment- muab tau los ntawm peptide uas nws cov yam ntxwv tseem ceeb suav nrog kev txhawb nqa kev qhia ntawm cov teeb meem neurotrophic (xws li BDNF), txhim kho synaptic plasticity, thiab tswj oxidative stress thiab neuroinflammation. Kev tshawb fawb feem ntau yog los ntawm kev mob stroke, hlwb raug mob, thiab kev paub txog kev ua haujlwm hauv Russia / Eastern Europe.

a.Receptors thiab Upstream Signaling: Feem ntau cov melanocortin receptor axis, nrog rau kev tsom mus rau MC4R; pib cAMP/PKA signaling.

b.Key Signaling Pathways: ERK/MAPK thiab PI3K/Akt tau raug soj ntsuam tas li kom qhib tau; downstream, lawv cuam tshuam cov kev hloov pauv xws li c-Fos thiab CREB, txhawb kev qhia txog cov kab mob neurotrophic (tshwj xeeb tshaj yog BDNF/TrkB axis).

c.Glial Cell Role: ERK/c-Fos ua kom zoo thiab ua kom zoo dua cytokine profiles tau pom nyob rau hauv astrocytes, qhia txog kev tiv thaiv tag nrho - kab mob.

d.Antioxidant/Cellular Protection: Muaj peev xwm ntawm Nrf2/HO-1 txoj kev, txo ROS thiab lipid peroxidation, alleviating excitotoxicity thiab ischemia-reperfusion raug mob.

e.Genetic Level: Cov ntaub ntawv sau tseg qhia txog kev hloov pauv ntawm cov noob muaj feem cuam tshuam nrog kev tsim kho synaptic / plasticity, o o, thiab kho axonal.

Pov Thawj Txheej txheem cej luam thiab ciam teb

a.In vitro: Hauv cov qauv neuronal / glial cell, nce kev ciaj sia, BDNF secretion, thiab ERK phosphorylation, thiab txo qis inflammatory thiab oxidative stress markers.

 

b.In vivo: Kev txhim kho ntawm tus cwj pwm thiab cov ntsiab lus ntawm histological tau rov qhia dua hauv ischemic stroke (xws li, MCAO), TBI, thiab cov qauv kev paub tsis meej.

 

c.Tam sim no kev txhais lus: kev siv tshuaj yog pom nyob rau hauv Russia thiab lwm cheeb tsam; Txawm li cas los xij, hauv ntau lub teb chaws / cheeb tsam, nws tseem yog cov ntaub ntawv tshawb fawb, thiab kev tshawb fawb ntxiv yog xav tau los kho kom ntev ntev -kev nyab xeeb thiab koob tshuaj- teb cov ntaub ntawv.

Application Scenarios thiab Endpoint Design

a. Neuroprotection/Plasticity: Hypoxia-reoxygenation, glutamate excitotoxicity, oxidative puas qauv; Cov ntsiab lus kawg suav nrog cell ciaj sia taus, cov cim synaptic, thiab qib neurotrophic yam tseem ceeb.
b. Neuroinflammation: LPS / cytokine stimulation; Kev kuaj pom ntawm NF-κB, Nrf2 axis, thiab inflammatory cytokine profiles (TNF- , IL-1 , IL-6).
c. Kev paub/kev coj tus cwj pwm: dej maze, paub cov khoom tshiab, Y-maze, qhib teb, thiab lwm yam.; combining histological (infarct ntim, neuron suav) thiab molecular endpoints (BDNF/ERK/Akt/CREB).
d. Omics thiab Mechanisms: RNA-seq/ATAC-seq, qPCR, WB, ELISA, immunofluorescence; ua ke nrog txoj kev inhibitors thiab receptor antagonists rau kev siv lub tshuab.

Cov lus pom zoo siv hauv vitro (kev siv ntau yam, yuav tsum tau ua kom zoo dua ntxiv raws li qhov project)

a. Concentration gradient: 10 nM-10 μM; Feem ntau siv thawj peb lub ntsiab lus: 100 nM, 300 nM, thiab 1 μM, los yog cov gradient zoo dua ntawm 0.1-1 μM.
b. Kev kho lub sij hawm: Pretreatment 30-60 min; Kev sib piv ntawm ob lub tswv yim: co-kev kho mob nrog kev ntxhov siab lossis kev kho mob ua ntej los ntawm kev ntxhov siab.
c. Tswj teeb: Sib npaug ntim tsis zoo tswj nrog vector; kev tswj zoo tuaj yeem yog foscorine lossis exogenous BDNF; Kev tswj hwm txoj cai tuaj yeem yog ERK inhibitor (U0126) lossis MC4R antagonist (xws li SHU9119).

Cov kev ceev faj

Siv cov khoom endotoxin tsawg thiab tsawg-cov khoom siv adsorption; txheeb xyuas kev sib raug zoo nrog cov ntshav / tshuaj tua kab mob / surfactants ua ntej.

Cim npe nrov: Tuam Tshoj semax peptide manufacturers, lwm tus neeg, Hoobkas