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Anticancer Drug

Our range of products include hertraz injection 440 mg, canmab injection and roch trastuzumab injection.

Hertraz Injection 440 mg

Hertraz Injection 440 mg
  • Hertraz Injection 440 mg
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Approx. Price: Rs 10 / PieceGet Latest Price

Product Details:

Minimum Order Quantity1 Piece
BrandHertraz
CompositionTrastuzumab
ManufacturerMylan
Treatmentbreast cancer and stomach cancer
PackagingVial Uses
Dosage Form440mg,150mg
Warning and PrecautionCommon side effectsNausea,Headache,Rash,Reduced blood platelets,Congestive cardiac failure
Dose440mg
UsageHospital, Personal, Clinical
Packaging SizeVial

Hertraz is a monoclonal antibody specifically designed to target HER2 receptors on breast cancer cells. It cancer cells for destruction by the body's immune system.The HER2 gene (also known as HER2/neu and ErbB2 gene) is amplified in 20–30% of early-stage breast cancers. Trastuzumab is a monoclonal antibody targeting HER2, inducing an immune-mediated response that causes internalization and downregulation of HER2. It may also upregulate cell cycle inhibitors such as p21Waf1 and p27Kip1.
The HER2 pathway promotes cell growth and division when it is functioning normally; however, when it is overexpressed, cell growth accelerates beyond its normal limits. In some types of cancer, the pathway is exploited to promote rapid cell growth and proliferation and hence tumor formation. The EGF pathway includes the receptors HER1 (EGFR), HER2, HER3, and HER4; the binding of ligands (e.g. EGF etc.). The pathway initiates the MAP kinase pathway as well as the PI3 kinase/AKT pathway, which in turn activates the NF-κB pathway. In cancer cells the HER2 protein can be expressed up to 100 times more than in normal cells (2 million versus 20,000 per cell). This overexpression leads to strong and constant proliferative signaling and hence tumor formation. Overexpression of HER2 also causes deactivation of checkpoints, allowing for even greater increases in proliferation. The HER receptors are proteins that are embedded in the cell membrane and communicate molecular signals from outside the cell (molecules called EGFs) to inside the cell, and turn genes on and off. The HER (human epidermal growth factor receptor) protein, binds to human epidermal growth factor, and stimulates cell proliferation. In some cancers, notably certain types of breast cancer, HER2 is over-expressed and causes cancer cells to reproduce uncontrollably. HER2 extends across the cell membrane, and carries signals from outside the cell to the inside. Signaling compounds called mitogens (specifically EGF in this case) arrive at the cell membrane, and bind to the extracellular domain of the HER family of receptors. Those bound proteins then link (dimerize), activating the receptor. HER2 sends a signal from its intracellular domain, activating several different biochemical pathways. These include the PI3K/Akt pathway and the MAPK pathway. Signals on these pathways promote cell proliferation and the growth of blood vessels to nourish the tumor (angiogenesis). Normal cell division—mitosis—has checkpoints that keep cell division under control. Some of the proteins that control this cycle are called cdk2 (CDKs). Overexpression of HER2 sidesteps these checkpoints, causing cells to proliferate in an uncontrolled fashion. This is caused by phosphorylation by Akt. Trastuzumab binds to domain IV of the extracellular segment of the HER2/neu receptor. Monoclonal antibodies that bind to this region have been shown to reverse the phenotype of HER2/neu expressing tumor cells. Cells treated with trastuzumab undergo arrest during the G1 phase of the cell cycle so there is reduced proliferation. It has been suggested that trastuzumab does not alter HER-2 expression, but downregulates activation of AKT. In addition, trastuzumab suppresses angiogenesis both by induction of antiangiogenic factors and repression of proangiogenic factors. It is thought that a contribution to the unregulated growth observed in cancer could be due to proteolytic cleavage of HER2/neu that results in the release of the extracellular domain. One of the most relevant proteins that trastuzumab activates is the tumor suppressor p27 (kip1), also known as CDKN1B. Trastuzumab has been shown to inhibit HER2/neu ectodomain cleavage in breast cancer cells. Experiments in laboratory animals indicate that antibodies, including trastuzumab, when bound to a cell, induce immune cells to kill that cell, and that such antibody-dependent cell-mediated cytotoxicity is another important mechanism of action.
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  • Packaging Details: 440mg , 150mg vial
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Canmab Injection

Canmab Injection
  • Canmab Injection
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Approx. Price: Rs 10 / PieceGet Latest Price

Product Details:

Minimum Order Quantity1 Piece
ManufacturerBiocon
BrandCanmab
Packagingvial
Dosage Form440mg
UsageClinical, Hospital
Strength440 mg
PackingVial

Trastuzumab, used to treat breast cancer and stomach cancer. It is specifically used for cancer that is HER2 receptor positive.The HER2 gene (also known as HER2/neu and ErbB2 gene) is amplified in 20–30% of early-stage breast Cancer. Trastuzumab is a monoclonal antibody targeting HER2, inducing an immune-mediated response that causes internalization and downregulation of HER2. It may also upregulate cell cycle inhibitors such as p21Waf1 and p27Kip1.
The HER2 pathway promotes cell growth, division when it is functioning normally however, when it is overexpressed, cell growth accelerates beyond its normal limits. In some types of cancer, the pathway is exploited to promote rapid cell growth and proliferation and hence tumor formation. The EGF pathway includes the receptors HER1 (EGFR), HER2, HER3, and HER4; the binding of ligands to HER receptors is required to activate the pathway. The pathway initiates the MAP kinase pathway as well as the PI3 kinase/AKT pathway, which in turn activates the NF-κB pathway. In cancer cells the HER2 protein can be expressed up to 100 times more than in normal cells (2 million versus 20,000 per cell). This overexpression leads to strong and constant proliferative signaling and hence tumor formation. Overexpression of HER2 also causes deactivation of checkpoints, allowing for even greater increases in proliferation.
The HER receptors are proteins that are embedded in the cell membrane and communicate molecular signals from outside the cell (molecules called EGFs) to inside the cell, and turn genes on and off. The HER (human epidermal growth factor receptor) protein, binds to human epidermal growth factor, and stimulates cell proliferation. In some cancers, notably certain types of breast cancer, HER2 is over-expressed and causes cancer cells to reproduce uncontrollably.
HER2 extends across the cell membrane, and carries signals from outside the cell to the inside. Signaling compounds called mitogens (specifically EGF in this case) arrive at the cell membrane, and bind to the extracellular domain of the HER family of receptors. Those bound proteins then link (dimerize), activating the receptor. HER2 sends a signal from its intracellular domain, activating several different biochemical pathways. These include the PI3K/Akt pathway and the MAPK pathway. Signals on these pathways promote cell proliferation and the growth of blood vessels to nourish the tumor (angiogenesis).
Normal cell division—mitosis—has checkpoints that keep cell division under control. Some of the proteins that control this cycle are called cdk2 (CDKs). Overexpression of HER2 sidesteps these checkpoints, causing cells to proliferate in an uncontrolled fashion. This is caused by phosphorylation by Akt.Trastuzumab binds to domain IV of the extracellular segment of the HER2/neu receptor. Monoclonal antibodies that bind to this region have been shown to reverse the phenotype of HER2/neu expressing tumor cells. Cells treated with trastuzumab undergo arrest during the G1 phase of the cell cycle so there is reduced proliferation. It has been suggested that trastuzumab does not alter HER-2 expre., but downregulates activation of AKT. In addition, trastuzumab suppresses angiogenesis both by induction of antiangiogenic factors and repression of proangiogenic factors. It is thought  a contribution to the unregulated growth observed in cancer could be due to proteolytic cleavage of HER2/neu that results in the release of the extracellular domain. One of the most relevant proteins that trastuzumab activates is the tumor suppressor p27 (kip1), also known as CDKN1B. Trastuzumab has been shown to inhibit HER2/neu ectodomain cleavage in breast cancer cells.
Experiments in lab animals indicated antibodies, including trastuzumab, when bound to a cell, induce immune cells to kill that cell, and that such antibody-dependent cell-mediated cytotoxicity is another important mechanism of action.
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  • Packaging Details: 440mg vial
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Roch Trastuzumab Injection

Roch Trastuzumab Injection
  • Roch Trastuzumab Injection
  • Roch Trastuzumab Injection
  • Roch Trastuzumab Injection
  • Roch Trastuzumab Injection
  • Roch Trastuzumab Injection
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Approx. Price: Rs 10 / PieceGet Latest Price

Product Details:

Minimum Order Quantity1 Piece
Packaging Size440mg,150mg
ManufacturerRoche
TreatmentHerceptin-trastuzumab-subcutaneous-intravenous-infusion-HER2-breast-cancer
Packaging440mg
Dosage Form440mg,150mg
BrandRoche
Dose Strength440mg,150mg
CategoryBreast Cancer
CompositionTrastuzumab
DrugTrastuzumab
Generic NameTrastuzumab
TypeInjection
Dose440 mg
Product TypeFinished Product
UsageClinical, Hospital, Personal
FormInjection
Side Effectof trastuzumab are flu-like symptoms (such as fever,chills and mild pain),nausea and diarrhea

Trastuzumab, sold under the brand name Herceptin among others, is a monoclonal antibody used to treat breast cancer. Specifically it is used for breast cancer that is HER2 receptor positive.It may be used by itself or together with other chemotherapy medication. Trastuzumab is given by slow injection into a vein and injection just under the skin.

Common side effects include fever, infection, cough, headache, trouble sleeping, and rash. Other severe side effects include heart failure, allergic reactions, and lung disease. Use during pregnancy may harm the baby. Trastuzumab works by binding to the HER2 receptor and slowing down cell duplication.

Trastuzumab was approved for medical use in the United States in 1998. It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.  A biosimilar was approved in the United States in 2018.
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