2. Metabolic Enzyme/Protease Stem Cell/Wnt MAPK/ERK Pathway PI3K/Akt/mTOR Apoptosis Cytoskeleton Cell Cycle/DNA Damage
  3. Herbicide ERK p38 MAPK JNK PI3K Akt Apoptosis Microtubule/Tubulin
  4. Dinitramine

Dinitramine is a herbicide. Dinitramine activates the Erk/P38/JNK/MAPK pathway and inactivates the PI3k/Akt pathway in testicular cells. Dinitramine induces endoplasmic reticulum stress, dysregulation of calcium homeostasis in the cytoplasm and mitochondria, apoptosis, and downregulated expression of cell cycle genes in testicular cells. Dinitramine reduces the viability and proliferation capacity of testicular cells, and inhibits cell division by suppressing the synthesis of tubulin. Dinitramine induces abnormal heart development, inhibited angiogenesis, inflammatory responses, apoptosis, and impaired embryonic growth in zebrafish embryos.

For research use only. We do not sell to patients.

Dinitramine

Dinitramine Chemical Structure

CAS No. : 29091-05-2

Size Stock
50 mg   Get quote  
100 mg   Get quote  
250 mg   Get quote  

* Please select Quantity before adding items.

This product is a controlled substance and not for sale in your territory.

Dinitramine Related Antibodies

Top Publications Citing Use of Products

View All ERK Isoform Specific Products:

View All Isoforms
ERK ERK1 ERK2 ERK5 ERK8

View All p38 MAPK Isoform Specific Products:

View All Isoforms
p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

View All JNK Isoform Specific Products:

View All Isoforms
JNK1 JNK2 JNK3 JNK

View All PI3K Isoform Specific Products:

View All Isoforms
PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

View All Akt Isoform Specific Products:

View All Isoforms
Akt Akt1 Akt2 Akt3

  • Biological Activity

  • Purity & Documentation

  • References

  • Customer Review

Description

Dinitramine is a herbicide. Dinitramine activates the Erk/P38/JNK/MAPK pathway and inactivates the PI3k/Akt pathway in testicular cells. Dinitramine induces endoplasmic reticulum stress, dysregulation of calcium homeostasis in the cytoplasm and mitochondria, apoptosis, and downregulated expression of cell cycle genes in testicular cells. Dinitramine reduces the viability and proliferation capacity of testicular cells, and inhibits cell division by suppressing the synthesis of tubulin. Dinitramine induces abnormal heart development, inhibited angiogenesis, inflammatory responses, apoptosis, and impaired embryonic growth in zebrafish embryos[1][2].

In Vitro

Dinitramine (2-20 μM; 24 h) reduces the viability and proliferative potential of TM3 and TM4 cells. Treatment with 20 μM dinitramine decreases the viability of TM3 cells to 78.7% and that of TM4 cells to 84.7%, and reduces the proliferative potential of both cell lines to below 50%[1].
Dinitramine (10-20 μM; 6 days) reduces the spheroid density and area of TM3 and TM4 cells in 3D culture systems; treatment with 20 μM decreases the spheroid density of TM3 cells by 22% and the area by 12%, while treatments with both 10 μM and 20 μM significantly reduce the spheroid density and area of TM4 cells[1].
Dinitramine (0-20 μM; 24 h) induces cell cycle arrest and cell death in TM3 and TM4 cells, inhibits the mRNA expression of cell cycle progression genes *Ccnd1*, *Cdk4* and *Ccne1* in cells, and activates endoplasmic reticulum stress in cells[1].
Dinitramine (0-20 μM) increases cytosolic and mitochondrial matrix calcium levels in TM3 and TM4 cells; treatment with 20 μM elevates the cytosolic calcium level to 230% in TM3 cells and to 300% in TM4 cells, while increasing the mitochondrial matrix calcium level to 230% in both cell lines[1].
Dinitramine (5-20 μM; 30 min) activates the Mapk signaling pathway and inactivates the Pi3k/Akt signaling pathway in TM3 and TM4 cells; treatment with 20 μM for 30 min upregulates the levels of phosphorylated Erk1/2, P38 and Jnk, while downregulates the levels of phosphorylated Akt and Rps6kb1 in both cell lines[1].
Combined treatment with dinitramine (20 μM; 24 h) and calcium regulators restores the proliferative potential of dinitramine-treated TM4 cells, but fails to restore that of TM3 cells[1].

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

Dinitramine Related Antibodies

Cell Viability Assay[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 0, 2, 5, 10, and 20 μM
Incubation Time: 24 h
Result: Reduced relative viability of TM3 cells to 78.7% and TM4 cells to 84.7% at 20 μM.
Reduced relative proliferative potential of TM3 and TM4 cells in a concentration-dependent manner to below 50% at 20 μM.

Cell Cycle Analysis[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 0, 2, 5, 10, and 20 μM
Incubation Time: 24 h
Result: Increased the number of TM3 and TM4 cells in the sub-G1 phase by approximately 2-fold compared to vehicle controls.
Reduced the number of TM4 cells in the G0/G1 phase by approximately 10%, with no remarkable changes in TM3 cell cycle phase distribution.

Real Time qPCR[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 20 μM
Incubation Time: 24 h
Result: Significantly reduced the expression of cell cycle progression-related genes Ccnd1, Cdk4, and Ccne1 in both TM3 and TM4 cells.

Western Blot Analysis[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 0, 5, 10, and 20 μM
Incubation Time: 24 h
Result: Increased Grp78/Bip protein expression in TM3 and TM4 cells in a concentration-dependent manner.
Increased Ire1α protein levels by 1.5-fold in TM3 and 2.4-fold in TM4 cells at 20 μM.
Increased phosphorylated Eif2α levels by 2.3-fold in TM3 and 1.4-fold in TM4 cells at 20 μM.
Increased Chop protein levels by 2.3-fold in TM3 and 2-fold in TM4 cells at 20 μM.

Western Blot Analysis[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 5-20 μM
Incubation Time: 30 min
Result: Increased phosphorylated Erk1/2 levels to 1.7-fold in TM3 and 1.9-fold in TM4 cells at 20 μM.
Increased phosphorylated P38 and Jnk levels significantly in both cell lines at 20 μM.
Reduced phosphorylated Akt levels to approximately half in TM3 cells and to 0.75-fold in TM4 cells at 20 μM.
Reduced phosphorylated Rps6kb1 levels to approximately half in TM3 cells and 0.59-fold in TM4 cells at 20 μM.
Reduced phosphorylated Rps6 levels to approximately half in TM3 cells (no significant change in TM4 cells) at 20 μM.

Cell Proliferation Assay[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 20 μM
Incubation Time: 24 h
Result: Restored proliferative potential of TM4 cells by approximately 20% compared to dinitramine alone when co-treated with 1 μM 2-APB.
Restored proliferative potential of TM4 cells to 65% compared to dinitramine alone when co-treated with 2 μM BAPTA.
Did not alter proliferative potential of dinitramine-treated TM3 cells with co-treatment.
In Vivo

Dinitramine (1.6-6.4 mg/L; water immersion; 96 h) induces concentration-dependent developmental toxicity, cardiotoxicity, vascular injury, inflammation and apoptosis in Danio rerio (zebrafish) embryos[2].

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

Animal Model: wild-type; fli1:eGFP transgenic[2]
Dosage: 1.6 mg/L; 3.2 mg/L; 6.4 mg/L
Administration: aqueous immersion; continuous exposure for 96 hours, medium refreshed every 24 hours
Result: Induced concentration-dependent malformations including shortened body length, reduced eye size, spinal curvature, swollen yolk sacs, and pericardial edema; increased pericardial edema to over 300% of control levels at 6.4 mg/L.
Reduced hatchability dose-dependently, reaching near 0% at 6.4 mg/L.
Decreased heart rate dose-dependently to 80 beats per minute at 6.4 mg/L (down from 184 bpm in controls); caused 3-fold enlargement of atrial long-axis diameter at 6.4 mg/L; significantly downregulated cardiac development genes (spaw, bmp4, bmp2b, erbb4b, myh6, itga5, lmna, actc1a, actc2) across all doses.
Reduced caudal vein plexus area to 80% of control and fluorescent intensity to 75% of control at 6.4 mg/L; caused abnormal formation of intersegmental vessels, dorsal longitudinal anastomotic vessel, dorsal aorta, and caudal vein; dysregulated expression of angiogenesis-related genes (kdr, vegfd, flt1, vegfaa).
Significantly upregulated inflammatory genes (il1b, nos2a, il6, tnfa, cox2a, cox2b) at 6.4 mg/L, with il1b expression increased 39-fold compared to controls.
Increased relative apoptotic cell numbers 4.8-fold (eye), 6.4-fold (brain), and 2.7-fold (tail) at 6.4 mg/L; upregulated pro-apoptotic genes (p53, casp8, casp9, casp3) and downregulated anti-apoptotic gene bcl2 across all doses.
Molecular Weight

322.24

Formula

C11H13F3N4O4
CAS No.
SMILES

NC1=C([N+]([O-])=O)C(N(CC)CC)=C(C=C1C(F)(F)F)[N+]([O-])=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
  • No file chosen (Maximum size is: 1024 Kb)
  • If you have published this work, please enter the PubMed ID.
  • Your name will appear on the site.

Dinitramine Related Classifications

  • Molarity Calculator

  • Dilution Calculator

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass   Concentration   Volume   Molecular Weight *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2
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:

Dinitramine29091-05-2HerbicideERKp38 MAPKJNKPI3KAktApoptosisMicrotubule/TubulinExtracellular signal regulated kinasesc-Jun N-terminal kinasePhosphoinositide 3-kinasePKBProtein kinase Bendoplasmic reticulum stresszebrafish embryosmicrotubulinErk/P38/Jnk Mapk pathwaycell cycleTM3 cellstesticular cellsPi3k/Akt pathwayTM4 cellsapoptosisherbicideInhibitorinhibitorinhibit

Your Recently Viewed Products:

Inquiry Online

Your information is safe with us. * Required Fields.

Product Name

  

Requested Quantity *

Applicant Name *

 

Salutation

Email Address *

 

Phone Number *

Department

 

Organization Name *

City

State

Country or Region *

      

Remarks

Bulk Inquiry

Inquiry Information

Product Name:
Dinitramine
Cat. No.:
HY-W714183
Quantity:
MCE Japan Authorized Agent:

Customer Review

Thank You for Your Feedback!

Request for HNMR Report

Please fill out this form to request the QC report. We will send it to your Email address shortly.

Your information is safe with us. * Required Fields.

Product Name

  

Lot #

Applicant Name *

 

Email Address *

Phone Number

 

Department *

Organization Name *

 

Country or Region *

Remarks

SAFETY DATA SHEET (SDS)

Request for HNMR Report

We have received your request and will respond to you as soon as possible.