| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| Other Sizes |
| Targets |
None (excipient). NT1-O12B interacts with transporters or receptors at the BBB (likely via the tryptamine headgroup mimicking neurotransmitters), enabling the lipidoid to cross the BBB. It also modulates immune signaling pathways, including inhibiting TLR8 activation.
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| ln Vitro |
A lipidoid with a tryptamine head group and a hydrophobic tail group with 12 carbon atoms is represented by the symbol NT1-O12B [1].
NT1-O12B exhibits immune-modulatory activity by inhibiting TLR8 activation, reducing the production of pro-inflammatory cytokines. It effectively encapsulates and delivers BBB-impermeable cargos across an in vitro BBB model (e.g., using bEnd.3 or hCMEC/D3 cell monolayers). Encapsulation of AmB (amphotericin B) in pure NT1-lipidoids (NT1-O12B) has been demonstrated. |
| ln Vivo |
Using a process akin to DiR encapsulation, it encapsulates AmB in pure NT1-lipoids (i.e., NT1-O12B, NT1-O14B, NT1-O16B, and NT1-O18B). Among all NT-lipoids, NT1-O12B exhibits the highest DiR fluorescence intensity, making it a dopant that improves brain delivery. The BBB-impermeable lipidoid PBA-Q76-O16B can be doped with NT1-O12B to produce an AmB formulation that is able to pass through the BBB. By using this technique, AmB concentrations in brain tissue reached 300 ng/g (AmB/tissue) less than 24 hours after AmB (5 mg/kg) was given intravenously, with a delivery efficiency of roughly 0.135% of the dose that was injected [1].
In vivo, NT1-O12B enhances cerebral delivery by intravenous injection when doped into otherwise BBB-impermeable LNPs. It has been used as an effective carrier for enhanced brain delivery of several BBB-impermeable cargos in mouse models. The NT1-O12B delivery system enables therapeutic cargos (e.g., antifungal agents) to penetrate the BBB, achieving therapeutic concentrations in the brain. |
| Enzyme Assay |
NT1-O12B (C3₆H₆0N2O4S4, MW 713.13) is dissolved in ethanol or DMSO. For BBB-penetrating LNP preparation, NT1-O12B is doped (typically at 10-30 mol%) into LNP formulations containing structural lipids (e.g., DOPC/DSPC, cholesterol) and an ionizable cationic lipid. The lipid mixture is combined with an aqueous solution containing cargo (e.g., AmB, siRNA, protein) via microfluidic mixing to form LNPs of ∼100 nm. Characterization includes DLS, zeta potential, encapsulation efficiency (>85%), and in vitro BBB permeability assessment using Transwell models with brain endothelial cells.
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| Cell Assay |
For in vitro permeability studies, brain endothelial cells (bEnd.3, hCMEC/D3) are cultured on Transwell inserts to form a tight BBB monolayer (TEER >200 omega·cm2). LNPs containing a fluorescent cargo (e.g., FITC-dextran, AmB-BODIPY) are added to the apical chamber. Permeability is measured by sampling the basolateral chamber and quantifying fluorescence at 0.5, 1, 2, 4, 6, and 24 h. The apparent permeability coefficient (Papp) is calculated, and an enhanced Papp (2-5-fold over control) indicates successful BBB crossing. Cellular uptake is assessed by flow cytometry. NT1-O12B-mediated TLR8 inhibition is evaluated in TLR8-expressing cells (e.g., HEK-Blue hTLR8). Cells are treated with NT1-O12B (0.1-100 uM) and a TLR8 agonist (e.g., R848), and NF-kappaB activation is measured via secreted embryonic alkaline phosphatase (SEAP) in the culture medium.
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| Animal Protocol |
For in vivo studies, LNPs containing NT1-O12B and a model cargo (e.g., fluorescent dye or AmB) are administered to BALB/c or C57BL/6 mice via intravenous (tail vein) injection at a total lipid dose of 10-50 mg/kg. Brain uptake is assessed 1-24 h post-dose. Mice are perfused transcardially with PBS to remove blood, and brains are harvested for fluorescence imaging, HPLC analysis, or tissue homogenization to quantify cargo concentration. For AmB delivery, brain fungal burden is measured in models of fungal meningitis. For immune modulation, plasma and brain levels of pro-inflammatory cytokines (e.g., IL-6, TNF-alpha) are measured by ELISA.
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| ADME/Pharmacokinetics |
No detailed PK data for NT1-O12B has been reported. NT1-O12B itself is not the therapeutic agent; it facilitates the PK behavior of the encapsulated cargo. NT1-O12B LNPs are designed to have a circulation half-life of approximately 2-4 h, sufficient for brain accumulation via passive targeting and active transport mechanisms. The lipidoid is expected to be metabolized into endogenous-like molecules (tryptamine and fatty acids), potentially reducing systemic toxicity.
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| Toxicity/Toxicokinetics |
In vitro, NT1-O12B shows low toxicity in brain endothelial cells (IC₅0 >100 uM). In vivo, NT1-O12B LNPs are well-tolerated at doses that achieve brain delivery (up to 50 mg/kg lipid i.v.) with no overt signs of neurotoxicity or systemic inflammation. The metabolic byproducts (tryptamine, fatty acids) are endogenous, supporting a favorable safety profile. However, comprehensive toxicology studies have not been published.
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| References | |
| Additional Infomation |
NT1-O12B (CAS 2739805-63-9, C3₆H₆0N2O4S4, MW 713.13) has >95% purity and is a pale yellow oil. Storage at -20degC is recommended. NT1-O12B belongs to a class of neurotransmitter-derived lipidoids (NT-lipidoids) that includes NT1-O14B, NT1-O16B, and NT1-O18B. These compounds are designed to facilitate BBB penetration and are not intended for direct therapeutic use. No clinical trials have been reported.
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| CAS # |
2739805-63-9
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| Appearance |
Colorless to light yellow ointment
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| Density |
1.124±0.06 g/cm3(Predicted)
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| Boiling Point |
780.1±60.0 °C(Predicted)
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| LogP |
0
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO: 200 mg/mL (280.45 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 5 mg/mL (7.01 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 50.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: 5 mg/mL (7.01 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 50.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 5 mg/mL (7.01 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
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.
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