2. Neuronal Signaling MAPK/ERK Pathway NF-κB Apoptosis Stem Cell/Wnt
  3. Tau Protein p38 MAPK NF-κB Apoptosis Bcl-2 Family ERK JNK
  4. Tau Protein Phosphorylation-IN-1

Tau Protein Phosphorylation-IN-1 is a tau protein phosphorylation inhibitor that potently protects PC12 cells against Aβ25–35-induced cytotoxicity (EC50 = 1.93 μM), and can penetrate the blood-brain barrier (BBB).Tau Protein Phosphorylation-IN-1 reverses the hyperphosphorylation of tau, significantly inhibits the expression of certain immune-related cytotoxic factors, suppresses the MAPK and NF-κB signaling pathways, and significantly inhibits the expression of RAGE and the apoptosis factors Bax/Bcl-2, both in vitro and in vivo. Tau Protein Phosphorylation-IN-1 relieves nerve damage, and improves learning and memory in an Alzheimer’s disease (AD) mouse model. Tau Protein Phosphorylation-IN-1 can be used for AD research.

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Tau Protein Phosphorylation-IN-1

Tau Protein Phosphorylation-IN-1 Chemical Structure

CAS No. : 3075165-36-2

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Tau Protein Phosphorylation-IN-1 Related Antibodies

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Description

Tau Protein Phosphorylation-IN-1 is a tau protein phosphorylation inhibitor that potently protects PC12 cells against Aβ25–35-induced cytotoxicity (EC50 = 1.93 μM), and can penetrate the blood-brain barrier (BBB).Tau Protein Phosphorylation-IN-1 reverses the hyperphosphorylation of tau, significantly inhibits the expression of certain immune-related cytotoxic factors, suppresses the MAPK and NF-κB signaling pathways, and significantly inhibits the expression of RAGE and the apoptosis factors Bax/Bcl-2, both in vitro and in vivo. Tau Protein Phosphorylation-IN-1 relieves nerve damage, and improves learning and memory in an Alzheimer’s disease (AD) mouse model. Tau Protein Phosphorylation-IN-1 can be used for AD research[1].

In Vitro

Tau Protein Phosphorylation-IN-1 (compound B1) (24 h) shows no toxicity in PC12 cells at 30 μM, and shows significant activity against Aβ25-35 (HY-P0128)-induced cytotoxicity in PC12 cells at 10 μM[1].
Tau Protein Phosphorylation-IN-1 (2.5-10 μM, 24 h) demonstrates multi-target neuroprotective effects in Aβ25-35-induced PC12 cells by significantly reducing tau phosphorylation at Thr181, Thr205, and Ser396, suppressing the phosphorylation of MAPKs (p38, ERK, JNK) and NF-κB, reversing the Aβ-induced upregulation of iNOS and COX-2, and modulating the expression of apoptosis-related proteins Bax and Bcl-2 alongside RAGE inhibition[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Tau Protein Phosphorylation-IN-1 Related Antibodies

Western Blot Analysis[1]

Cell Line: PC12 cells
Concentration: 2.5, 5 and 10 μM
Incubation Time: 24 h
Result: Decreased phosphorylated tau levels at Thr181, Thr205, and Ser396 sites caused by Aβ25–35 compared to the model group.
Exhibited stronger inhibition of tau phosphorylation at the Thr181, Thr205, and Ser396 sites than Oleanolic acid (OA)(HY-N0156) or Donepezil (HY-14566) at 10 μM.
Reversed the Aβ25–35-induced upregulation of iNOS and COX-2 levels.
Significantly inhibited RAGE expression at 5 and 10 μM.
Decreased Bax and Bcl-2 expression compared to the control group.
Inhibited the phosphorylation of p38 MAPK, ERK and JNK, thereby blocking the MAPK signaling pathway.
Reduced the expression of p-NF-κB in Aβ25–35-induced PC12 cells.
In Vivo

Tau Protein Phosphorylation-IN-1 (2.5, 5 and 10 mg/kg, i.p., daily for 28 days) rescues cognitive deficits, attenuates tau hyperphosphorylation, and suppresses neuroinflammation in an AD mouse model[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male ICR mice (20-22 g) intracerebroventricularly injected with Aβ₂₅–₃₅ solution (9 nmol/3 μL/mouse) [1]
Dosage: 2.5, 5 and 10 mg/kg
Administration: i.p., daily for 28 days
Result: Reduced the escape latencies on training days 2-5 compared with the Aβ group in the Morris water maze test.
Increased the number of crossings over the original platform location, in contrast to the significant reduction observed in the Aβ group.
Reversed the Aβ-induced histopathological damage, including irregular neuronal distribution and reduced cell numbers in the hippocampal CA1 and CA3 areas.
Significantly reduced the levels of tau phosphorylation at Thr205, and Ser396 sites, compared with the Aβ group.
Significantly decreased the level of tau phosphorylation at the Thr181 site in the hippocampus, especially in the DG, CA1, and CA3 pyramidal neurons.
Suppressed the Aβ25-35-induced upregulation of iNOS, COX-2, RAGE, and the Bax/Bcl-2 ratio.
Showed an inhibitory effect on p38 MAPK, ERK, and JNK phosphorylation in Aβ25-35-induced AD mice.
Inhibited the Aβ25-35-induced upregulation of NF-κB in a dose-dependent manner.
Caused no histopathological damage in the liver or kidneys at any tested dose (up to 10 mg/kg) over 21 days.
Molecular Weight

628.89

Formula

C39H56N4O3
CAS No.
SMILES

O=C([C@]12[C@](CC(C)(CC2)C)([H])C3=CC[C@@]([C@@]4([C@@](C(C)([C@H](CC4)O)C)([H])CC5)C)([H])[C@]5(C)[C@@]3(CC1)C)OCCN6C(C7=CC=CC=C7)=NN=N6
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Tau Protein Phosphorylation-IN-1 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Tau Protein Phosphorylation-IN-13075165-36-2Tau Proteinp38 MAPKNF-κBApoptosisBcl-2 FamilyERKJNKNuclear factor-κBNuclear factor-kappaBExtracellular signal regulated kinasesc-Jun N-terminal kinasetau proteinblood-brain barrierAβ25–35-induced PC12 cellshyperphosphorylationMAPKRAGEapoptosisADAβ25–35-induced AD miceInhibitorinhibitorinhibit

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