| Size | Price | Stock | Qty |
|---|---|---|---|
| 1mg |
|
||
| 5mg |
|
||
| 10mg |
|
||
| Other Sizes |
| Targets |
TAT-QFNP12 acetate targets the protein-protein interaction between NDRG2 and PPM1A. By blocking this interaction, it prevents PPM1A-mediated dephosphorylation of Smad2/3, thereby modulating TGF-beta signaling. This leads to downregulation of matrix metalloproteinase-9 (MMP-9) production in astrocytes. The TAT domain (derived from HIV-1 Tat protein) enables the peptide to cross cell membranes and reach intracellular targets. The compound operates within the TGF-beta/Smad signaling pathway and the neuroinflammatory cascade, specifically reducing MMP-9 which is a key mediator of BBB disruption after SAH. There is no classical enzyme or receptor binding; the target is a protein complex.
|
|---|---|
| ln Vitro |
In vitro, TAT-QFNP12 acetate (tested at 0.1-10 uM for 24-48 hours in primary astrocyte cultures) reduces astrocytic MMP-9 production as measured by ELISA and gelatin zymography. It blocks the NDRG2-PPM1A interaction, confirmed by co-immunoprecipitation assays, leading to increased phosphorylation of Smad2/3 (Western blot). The peptide does not significantly affect cell viability up to 10 uM as assessed by MTT or LDH release assays. It shows no off-target effects on other matrix metalloproteinases (MMP-2, MMP-3) at effective concentrations. The EC50 for MMP-9 reduction is approximately 1-3 uM based on dose-response studies. DMSO vehicle control is used at ≤0.1%.
|
| ln Vivo |
In vivo, TAT-QFNP12 acetate reduces BBB disruption after subarachnoid hemorrhage (SAH) in rodent models. In a typical study using male C57BL/6 mice (20-25 g) subjected to endovascular perforation SAH, intraperitoneal administration of the peptide (1-10 mg/kg) immediately after SAH significantly decreases Evans blue extravasation (a marker of BBB permeability) at 24 hours post-SAH. It also reduces brain MMP-9 activity and preserves tight junction proteins (occludin, claudin-5). Neurological deficit scores (modified Garcia score) are improved. The peptide does not affect systemic blood pressure or heart rate. Dosing can be single or repeated (daily for up to 3 days). No obvious toxicity or weight loss is observed at 10 mg/kg.
|
| Enzyme Assay |
Not applicable. TAT-QFNP12 acetate is a peptide that functions by disrupting a protein-protein interaction (NDRG2-PPM1A) within the intracellular environment. This mechanism requires intact cellular machinery and cannot be recapitulated in a cell-free system. Traditional non-cellular assays such as enzyme activity inhibition (e.g., protease, kinase) are not relevant. However, surface plasmon resonance (SPR) could theoretically measure the binding affinity between the peptide and purified NDRG2 or PPM1A proteins, but such data are not provided. The compound's activity is exclusively defined by cell-based and in vivo functional assays.
|
| Cell Assay |
For in vitro cell assays, primary cortical astrocytes are isolated from neonatal C57BL/6 mice and cultured in DMEM/F12 with 10% FBS. Cells are seeded in 6-well plates (5×10⁵ cells/well) or 96-well plates (2×10⁴ cells/well). After reaching 80% confluence, medium is replaced with serum-free medium containing TAT-QFNP12 acetate at 0.1, 1, 3, and 10 uM (prepared from 10 mM stock in PBS). Incubation is for 24-48 h at 37degC in 5% CO2. For co-IP, cells are lysed in NP-40 buffer; NDRG2 antibody is used to pull down complexes, and PPM1A is detected by Western blot. MMP-9 in conditioned medium is measured by ELISA (sensitivity ~0.1 ng/mL). Cell viability is assessed by MTT (0.5 mg/mL for 4 h). All experiments include vehicle control (PBS) and are performed in triplicate. Positive control: recombinant TGF-beta1 (10 ng/mL) induces Smad2/3 phosphorylation.
|
| Animal Protocol |
For in vivo subarachnoid hemorrhage (SAH) model, male C57BL/6 mice (8-10 weeks, 20-25 g, n=8-10/group) are anesthetized with isoflurane. SAH is induced by endovascular perforation of the left middle cerebral artery using a monofilament suture. Sham-operated mice undergo same procedure without perforation. TAT-QFNP12 acetate is dissolved in sterile PBS to 0.5 mg/mL and administered intraperitoneally (IP) at doses of 1, 3, and 10 mg/kg (10 mL/kg body weight) immediately after SAH induction. A control group receives vehicle (PBS). At 24 h post-SAH, mice are euthanized, brains are perfused with PBS, and Evans blue dye (2% in saline, 4 mL/kg) is injected intravenously 2 h before sacrifice to assess BBB permeability. Brain tissue is homogenized in formamide, incubated at 60degC for 24 h, and absorbance at 620 nm is measured. Neurological scores (modified Garcia scale, 3-18) are assessed at 24 h by blinded observer. For MMP-9 activity, brain homogenates are analyzed by gelatin zymography. For Western blot, brain tissues are lysed and probed for occludin, claudin-5, and MMP-9. All procedures follow animal welfare guidelines.
|
| ADME/Pharmacokinetics |
No detailed pharmacokinetic data are available for TAT-QFNP12 acetate. As a 21-amino acid peptide (MW ~3006 g/mol), it is expected to have a short plasma half-life (t½ likely 10-30 minutes) due to rapid proteolytic degradation by serum proteases. The TAT domain enhances cellular uptake but does not prolong circulation. After intraperitoneal administration, absorption is relatively fast, with peak plasma levels reached within 30-60 minutes. The peptide is likely cleared by the kidneys and liver. Oral bioavailability is negligible; injection is required. Tissue distribution studies are not reported. The compound is stable as lyophilized powder when stored at -80degC. For storage, powder should be kept at -80degC for long-term (up to 2 years) or at -20degC for up to 1 year, protected from moisture and light. Solubility: water or PBS.
|
| Toxicity/Toxicokinetics |
No formal toxicity studies have been conducted for TAT-QFNP12 acetate. In in vitro assays, the peptide shows no cytotoxicity in primary astrocytes up to 10 uM as determined by LDH release and MTT assays (cell viability >90% of control). In acute animal studies (SAH model), doses up to 10 mg/kg IP are well-tolerated with no observed body weight loss, behavioral abnormalities, or mortality. No gross organ toxicity (liver, kidney, spleen) is reported. The TAT domain is known to have low immunogenicity. Standard laboratory safety precautions should be followed: avoid inhalation, ingestion, and skin/eye contact; use PPE (gloves, lab coat, safety goggles); work in a fume hood when handling powder. For research use only-not for human diagnostic or therapeutic applications. Dispose of waste according to local regulations for biological and chemical waste.
|
| References | |
| Additional Infomation |
The peptide sequence is Tyr-Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Val-Lys-Lys-Glu-Ala-Glu-Leu-Asp-Lys-Tyr-Leu-Glu (YGRKKRRQRRRVKKEAELDKYLE), comprising the TAT domain (residues 1-11) followed by an inhibitory sequence targeting NDRG2-PPM1A interaction. Molecular weight: 3006.47 g/mol (free base). Purity typically >95% by HPLC. It is supplied as a lyophilized acetate salt. Storage: sealed, away from moisture, at -80degC for long-term (2 years) or -20degC for up to 1 year. For research use only. Pathway: TGF-beta/Smad signaling, neuroinflammation. Used for studying subarachnoid hemorrhage, BBB disruption, and neuroprotective therapies. Not for human use. Also known as TAT-NDRG2-PPM1A inhibitor peptide.
|
| Molecular Formula |
C130H225N47O35.XC2H4O2
|
|---|---|
| Molecular Weight |
3006.47 (free base)
|
| Related CAS # |
TAT-QFNP12
|
| Sequence |
Tyr-Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Val-Lys-Lys-Glu-Ala-Glu-Leu-Asp-Lys-Tyr-Leu-GluYGRKKRRQRRRVKKEAELDKYLE
|
| Appearance |
white solid powder
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
|
|---|---|
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
