CJC 1295 tshuaj tsuagyog tshuaj tsuag tshuaj raws li CJC-1295 peptide hormone. Nws yog ib qho kev sib txuas ntawm kev loj hlob hormone tso tawm hormone (GHRH) analogue, muaj 30 amino acid residues. Los ntawm kev hloov kho molecular tshwj xeeb, nws ib nrab - lub neej hauv lub cev tau txuas ntxiv, mus txog 6-8 hnub. Qhov no ntev - tus yam ntxwv kav ntev ua rau nws txuas ntxiv txhawb kev tso tawm ntawm kev loj hlob hormone (GH) los ntawm cov qog pituitary anterior, yog li txhawb kev tsim cov tshuaj insulin-zoo li kev loj hlob Factor-1 (IGF1) hauv daim siab, uas muaj kev cuam tshuam dav rau cov kab mob hauv lub cev.
Lub ntsiab zoo ntawm Spray dag nyob rau hauv nws yooj yim siv thiab ruaj khov tso tshuaj. Kev npaj tshuaj tsuag tso cai rau cov tshuaj sai sai nqus los ntawm cov mucosa, zam qhov tsis yooj yim thiab mob tshwm sim los ntawm kev txhaj tshuaj, thiab txhim kho tus neeg mob txoj kev ua raws cai. Nyob rau tib lub sijhawm, kev saib xyuas lub sijhawm ntev ntawm GH thiab IGF1 ruaj khov yog ntau dua raws li txoj cai ntawm lub cev, kom tsis txhob muaj kev tawm tswv yim tsis zoo los ntawm kev siv tshuaj hormone exogenous.
Peb Cov Khoom Muag Khoom








CJC-1295 COA


CJC 1295 tshuaj tsuagyog ib qho kev tsim tawm kev loj hlob hormone tso tawm cov tshuaj hormones (GHRH) analog tsim los ntawm Canadian biotechnology tuam txhab ConjuChem los ntawm cov txheej txheem molecular engineering. Cov txheej txheem tseem ceeb khaws cia thaj chaw lom neeg lom zem (1-29 amino acids) ntawm ntuj GHRH, thiab ib nrab- lub neej txuas ntxiv mus rau 8 hnub dhau los ntawm kev hloov kho tshuaj affinity complex (DAC) thev naus laus zis, ua tiav cov tshuaj tiv thaiv kev tso tawm. Hauv kev kho cov ntaub so ntswg thiab cov tshuaj kho dua tshiab, tswj kev tso tawm ntawm cov tshuaj hormones loj hlob (GH) thiab insulin-zoo li kev loj hlob zoo tshaj plaws-1 (IGF1) txhawm rau qhib cov tshuab kho endogenous tau pom tias muaj peev xwm ntau rau daim ntawv thov.
Kev kho daim tawv nqaij: pab txhawb kev rov tsim dua tshiab thiab caws pliav
1. Kho qhov txhab mob
Los ntawm kev tswj hwm qib ntawm IGF1, nws tuaj yeem txhawb nqa kev loj hlob ntawm keratinocytes thiab fibroblasts, thiab ua kom cov kab mob rov ua dua ntawm cov qhov txhab mob ntev (xws li mob ntshav qab zib ko taw rwj thiab venous ulcers). Kev tshawb fawb soj ntsuam pom tau hais tias kev siv tshuaj tsuag hauv zos tuaj yeem txo lub sijhawm kho mob ntshav qab zib ko taw rwj los ntawm 40% thiab nce tus nqi kho tau los ntawm 35%. Lub tshuab muaj xws li:
IGF1 signaling activation: IGF1 activates PI3K / Akt txoj kev los ntawm kev khi rau epidermal sytes membrane receptors, txhawb sytes migration thiab proliferation.
Collagen metabolic tshuav nyiaj li cas: inhibiting kev xa ntawm matrix metalloproteinase (MMP) -9, txo collagen degradation, thaum upregulating cov kev ua ntawm collagen synthase (xws li LOX), txhim kho caws pliav elasticity.
Angiogenesis: GH / IGF1 axis pab txhawb kev mob microvascular tsim thiab txhim kho cov ntshav hauv zos los ntawm kev txhawb nqa cov khoom ntawm vascular endothelial kev loj hlob (VEGF).

2. Kev kho pob txuv
Hauv kev kho cov nti tom qab kub hnyiab lossis raug mob, tswj TGF - /Smad txoj hauv kev inhibits qhov sib txawv ntawm fibroblasts rau hauv myofibroblasts thiab txo cov collagen ntau dhau. Cov kev sim tsiaj tau pom tias kev txhaj tshuaj hauv zos tuaj yeem txo qhov caws pliav los ntawm 50%, caws pliav tawv los ntawm 60%, thiab txhim kho caws pliav xim thiab kev ntxhib los mos.
3. Daim tawv nqaij tiv thaiv -aging
Los ntawm kev ua kom lub GH / IGF1 axis, nws pab txhawb cov synthesis ntawm collagen thiab elastin nyob rau hauv dermal fibroblasts, txo UV induced photoaging puas. Kev soj ntsuam kev soj ntsuam pom tau tias tom qab 8 lub lis piam ntawm kev siv tshuaj tsuag tas li, daim tawv nqaij elasticity ntawm cov neeg mob tau nce los ntawm 25%, qhov tob tob zuj zus los ntawm 30%, thiab epidermal thickness nce 15%.

Cov pob txha thiab pob txha rov tsim dua tshiab: kho cov pob txha tsis xws luag thiab cov kab mob sib koom ua ke degenerative

1. Kho pob txha
Ua kom nrawm kho pob txha los ntawm cov tshuab hauv qab no:
Refined pob txha tsim: GH / IGF1 axis activates osteoblast sib txawv, upregulates cov khoom ntawm pob txha morphogenetic protein-2 (BMP) thiab Runx2, thiab pab txhawb cov pob txha matrix synthesis.
Cov pob txha resorption inhibition: Downregulate osteoclast kev ua si, txo cov qib ntawm cov pob txha resorption cim (xws li CTX-I), thiab tswj cov pob txha metabolism.
Kev nce qib Angiogenesis: IGF1 upregulates VEGF conveys, txhim kho cov ntshav txaus rau qhov chaw tawg, thiab muab khoom noj khoom haus rau kev kho pob txha.
Kev tshawb fawb soj ntsuam qhia tau hais tias hauv zos daim ntawv thov ntawmCJC 1295 tshuaj tsuagtuaj yeem txo lub sijhawm kho ntawm tibial pob txha los ntawm 3 lub lis piam, thiab kev kho kom zoo (xws li pob txha ntom ntom thiab cov qauv trabecular) yog qhov zoo dua li ntawm pawg tswj hwm.
2. Kev kho mob osteoarthritis
Nyob rau hauv tus qauv osteoarthritis (OA), degeneration ntawm pob txha pob txha caj qaum yog ncua los ntawm inhibiting chondrocyte apoptosis thiab matrix degradation:
Kev tiv thaiv pob txha mos: Downregulate cov khoom ntawm MMP-13 thiab ADAMTS-5, txo collagen II thiab proteoglycan degradation.
Cov nyhuv tiv thaiv kab mob: GH / IGF1 axis inhibits qhov kev tso tawm ntawm pro-inflammatory yam xws li IL-1 thiab TNF - , txo cov synovial o.
Synovial kho: Ua kom cov synovial sytes proliferation thiab txhim kho kev sib koom ua ke lubrication muaj nuj nqi.
Cov kev sim tsiaj tau pom tias kev txhaj tshuaj intra- articular txhaj tuaj yeem ua rau cov pob txha pob txha tuab ntawm 40% thiab txhim kho cov qhab nia ua haujlwm sib koom ua ke los ntawm 50% hauv OA qauv nas.
3. Kho pob txha kho
Rau cov pob txha loj lossis tsis muaj kev sib koom ua ke, kev sib xyaw ntawm cov pob txha graft cov ntaub ntawv xws li hydroxyapatite thiab - tricalcium phosphate tuaj yeem txhim kho kev kho kom zoo. Lub tshuab muaj xws li:
Osteogenesis induction: Los ntawm kev ua kom Wnt / - catenin txoj hauv kev, nws pab txhawb kev sib txawv ntawm cov pob txha pob txha mesenchymal qia sytess (BMSCs) rau hauv osteoblasts.
Angiogenesis: IGF1 upregulates cov khoom ntawm hypoxia inducible factor (HIF) -1, inducing endothelial sytes migration thiab lumen tsim.
Cov pob txha integration refinement: Txhim kho lub microenvironment ntawm cov pob txha implant interface thiab pab txhua yam anchoring ntawm pob txha cov ntaub so ntswg thiab cov khoom cog.
Cov kws kho mob tau pom tias kev sib xyaw ua ke ntawm CJC-1295 thiab kev hloov cov pob txha autogenous rau kev kho mob ntawm tibial pob txha tsis xws luag tau nce tus nqi kho tau los ntawm 65% mus rau 90% thiab txo lub sijhawm kho los ntawm 50%.
Kev Kho Cov Muscle: Ua kom rov qab los ntawm Kev Ua Si Ua Si thiab Kho Cov Muscle Atrophy

1. Kev kho mob kis las
CJC-1295 pab txhawb kev kho cov leeg nqaij los ntawm txoj hauv kev hauv qab no:
Satellite sytes activation: GH / IGF1 axis activates cov leeg nqaij satellite sytes proliferation thiab sib txawv, rov ua kom puas cov nqaij fibers.
Anti-inflammatory thiab antioxidant: CJC-1295 inhibits NF - κ B txoj hauv kev, txo cov kev tso tawm ntawm cov kab mob xws li IL-6 thiab TNF - , thiab txhawb kev ua haujlwm ntawm superoxide dismutase (SOD) kom txo tau cov kev ntxhov siab oxidative puas tsuaj.
Cov nqaij fiber ntau rov tsim dua tshiab: IGF1 qhib txoj hauv kev mTOR, ua kom cov nqaij protein synthesis, thiab ua kom rov qab tau cov nqaij fiber ntau hla - ntu ntu.
Kev tshawb fawb soj ntsuam pom tau hais tias tom qab siv tshuaj tsuag hauv zos, lub sij hawm rov qab los ntawm quadriceps strain yog luv luv los ntawm 40% thiab qhov rov zoo ntawm cov leeg nqaij yog nce 35%.
2. Kev kho cov leeg nqaij atrophy
Hauv kev tsis siv cov leeg nqaij atrophy (xws li ntev - so lub sijhawm pw, kev raug mob qaum qaum) lossis kab mob - cuam tshuam cov leeg nqaij atrophy (xws li mob qog noj ntshav cachexia, kab mob pulmonary mob ntev), cov leeg poob yog thim rov qab los ntawm cov tshuab hauv qab no:
Anti catabolic metabolism: inhibits ubiquitin proteasome system (UPS) thiab autophagy lysosome txoj kev, txo cov leeg nqaij protein degradation.
Txhawb nqa cov metabolism hauv hluavtaws: GH / IGF1 axis activates PI3K / Akt / mTOR txoj hauv kev, txhawb cov leeg nqaij protein synthesis thiab nqaij fiber ntau hypertrophy.
Kev txhim kho ntawm mitochondrial muaj nuj nqi: Upregulation ntawm PGC-1 qhia refines mitochondrial biogenesis thiab oxidative phosphorylation muaj peev xwm, thiab txhim kho cov leeg nqaij zog metabolism efficiency.
Cov kev sim tsiaj tau pom tias kev kho mob tuaj yeem ua rau cov leeg nqaij quadriceps nce 50% thiab rov qab kho tus ntoo khaub lig- ntu ntu ntawm cov leeg nqaij mus rau 80% ntawm cov qib ib txwm nyob rau hauv cov leeg nqaij atrophy nas.

Neural regeneration: txhawb kev kho cov hlab ntsha peripheral
1. Kho cov hlab ntsha peripheral raug mob
Yooj yim rau peripheral paj regeneration los ntawm cov tshuab hauv qab no:
Schwann sytes proliferation: GH / IGF1 axis activates Schwann sytes migration thiab myelination, muab kev taw qhia thiab kev txhawb nqa rau axonal regeneration.
Upregulation ntawm neurotrophic yam conveying: pab txhawb lub synthesis ntawm paj hlwb kev loj hlob (NGF), lub paj hlwb - muab tau neurotrophic yam (BDNF), thiab glial sytes derived neurotrophic yam (GDNF), pab txhawb neuronal ciaj sia taus thiab axonal extension muaj peev xwm.
Kev tiv thaiv kab mob thiab tiv thaiv caws pliav: Inhibit TGF - 1 conveying, txo peripheral fibrosis, thiab txhim kho microenvironment ntawm paj hlwb regeneration.
Cov kev tshawb fawb soj ntsuam pom tau tias tom qab siv hauv zosCJC 1295 tshuaj tsuagHauv cov neeg mob uas raug mob sciatic hlab ntsha, qhov rov qab ntawm cov hlab ntsha ntawm cov hlab ntsha tau nce los ntawm 40%, thiab qib ntawm cov leeg nqaij atrophy txo qis los ntawm 30%.


2. Kev kho tus txha caj qaum
Hauv cov qauv kev raug mob ntawm tus txha caj qaum, cov teebmeem neuroprotective raug siv los ntawm cov hauv qab no:
Anti inflammatory thiab antioxidant: inhibits qhov ua kom microglia, txo qhov tso tawm ntawm IL-1 thiab TNF - , thaum upregulating glutathione (GSH) qib kom txo oxidative kev nyuaj siab puas.
Neurogenesis nce qib: GH / IGF1 axis activates endogenous neural qia sytes proliferation thiab sib txawv, replenishing puas neurons.
Kev txhim kho ntawm synaptic plasticity: Upregulation ntawm synaptophysin thiab kev loj hlob txuam nrog protein (GAP) -43 conveying pab txhawb synaptic remodeling thiab functional rov qab.
Tsiaj thwmsim tau pom tias kev kho mob tuaj yeem nce hind limb lub cev muaj zog cov qhab nia los ntawm 50% thiab txo qis qaum qaum hauv cheeb tsam los ntawm 40% hauv cov nas nrog tus txha caj qaum raug mob.
Kev kho mob: optimizing cov txheej txheem ntawm kev kho qhov txhab mob
1. Kho qhov txhab mob
Ua kom nrawm ntawm kev kho mob ntawm qhov txhab mob (xws li phais phais thiab abrasions) los ntawm cov tshuab hauv qab no:
Kev tswj cov kab mob inflammatory: Cov ntawv thov thaum ntxov tuaj yeem cuam tshuam cov neutrophil infiltration, txo qhov txhab exudation, thiab pab txhawb macrophage polarization ntawm M2 hom, secreting kho kev txhawb nqa yam xws li IL-10 thiab TGF - 1.
Kev nce qib: txhawb kev loj hlob ntawm fibroblasts thiab endothelial sytess, accelerates granulation ntaub so ntswg tsim thiab angiogenesis.
Reshaping optimization: Los ntawm kev tswj hwm collagen metabolism tshuav nyiaj li cas, CJC-1295 txo cov caws pliav thiab txhim kho qhov txhab thiab ua haujlwm.
Kev soj ntsuam kev soj ntsuam tau pom tias tom qab siv hauv zos ntawm kev phais mob plab, lub sijhawm kho tau luv los ntawm 3 hnub thiab qhov caws pliav dav txo los ntawm 50%.

2. Kev kho mob ntawm qhov txhab
Hauv cov kab mob sib kis (xws li kub hnyiab qhov txhab thiab mob ntshav qab zib ko taw), CJC-1295 ua kom nws lub peev xwm tiv thaiv kab mob los ntawm cov hauv qab no:
Kev tswj kev tiv thaiv kab mob: GH / IGF1 axis activates neutrophil thiab natural killer (NK) sytes ua haujlwm, txhim kho cov kab mob tshem tawm.
Upregulation ntawm antimicrobial peptide conveying: pab txhawb lub secretion ntawm Defensin thiab Catelicidin los ntawm keratinocytes, ncaj qha tua cov kab mob.
Biofilm cuam tshuam: IGF1 inhibits biofilm tsim thiab refines tshuaj tua kab mob permeability los ntawm downregulating cov kab mob quorum sensing system.
Cov kev sim tsiaj tau pom tias kev siv tshuaj tua kab mob ua ke tuaj yeem txo qhov hnyav ntawm Staphylococcus aureus hauv qhov txhab kub hnyiab los ntawm 90% thiab nce tus nqi kho tau los ntawm 60%.
Kev kho kev laus los tiv thaiv kev laus: thim rov qab lub hnub nyoog- cuam tshuam cov ntaub so ntswg degeneration
Stem cell activation
Ua kom endogenous qia sytess los ntawm cov tshuab hauv qab no:
Hematopoietic qia sytess: GH / IGF1 axis pab txhawb kev loj hlob ntawm hematopoietic qia sytess thiab txhim kho lub cev tiv thaiv kab mob ntawm cov neeg laus.
Mesenchymal qia sytess: Upregulation ntawm CXCR4 qhia refines lub peev xwm ntawm qia sytess migrate rau cov ntaub so ntswg puas.
Neural qia sytess: IGF1 pab txhawb kev sib txawv ntawm neural qia sytess rau hauv neurons thiab txhim kho kev txawj ntse los ntawm kev ua kom txoj hauv kev Notch.
Cov kev sim tsiaj tau pom tiasCJC 1295 tshuaj tsuagKev kho mob tuaj yeem nce tus naj npawb ntawm cov neurons hauv hippocampus ntawm cov neeg laus nas los ntawm 40% thiab txhim kho qhov muaj peev xwm nco tau zoo.
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