Depofoam Technology; Proprietary Technology of Pacira Pharmaceuticals

DepoFoam^® consists of microscopic, spherical, lipid-based particles composed of a honeycomb of numerous, non-concentric, internal aqueous chambers containing the encapsulated drug. Each chamber is separated from adjacent chambers by lipid membranes. Following injection, the DepoFoam particles release the drug over an extended period of time due to erosion and/or reorganization of the lipid membranes. 

DepoFoam permits systemic delivery of medications by releasing the drug into the bloodstream via the interstitial space. Locally, DepoFoam can release the drug into a body compartment, such as a joint.

Both small and large molecule compounds can successfully be encapsulated into DepoFoam, including:

• Traditional injectable pharmaceuticals
• Proteins
• Peptides
• Antisense oligonucleotides
• DNA

DepoFoam has been used in two FDA-approved commercial products, including DepoCyt(e)^® (cytarabine liposome injection), EXPAREL^® (bupivacaine liposome injectable suspension).

Reference:

 

http://www.pacira.com

Acticoat* ; Antimicrobial Barrier Dressing

Acticoat* (with Nanocrystalline Silver) ^† dressing is an effective antimicrobial barrier dressing. The nanocrystalline coating of silver rapidly kills a broad spectrum of bacteria in as little as 30 minutes. Acticoat dressing consists of three layers: an absorbent inner core sandwiched between outer layers of silver coated, low adherent polyethylene net. Nanocrystalline silver protects the wound site from bacterial contamination while the inner core helps maintain the moist environment optimal for wound healing.

 

Acticoat is an effective barrier to over 150 pathogens which includes a broad spectrum of gram positive and gram negative bacteria and fungal wound pathogens. Acticoat is an effective barrier to antibiotic-resistant bacteria such as Antibiotic-resistant Pseudomonas, Methicillin-resistant Staphylococcus aureus (MRSA) and Vancomycin-resistant Enterococcus (VRE).  

References:

http://www.smith-nephew.com/australia/healthcare/products/product-types/antimicrobial-dressings/silver-dressings/acticoat--product-range/acticoat-/

                                               -HAVE A GOOD DAY-

Avastin; angiogenesis inhibitor for chemotherapy

Avastin (Bevacizumab) is approved for:

• Metastatic colorectal cancer (mCRC) 
• Advanced nonsquamous non–small cell lung cancer (NSCLC) in combination with carboplatin and paclitaxel in people who have not received chemotherapy for their advanced disease.
• Metastatic kidney cancer (mRCC) when used with interferon alfa.
• Glioblastoma (GBM) when taken alone in adult patients whose cancer has progressed after prior treatment. The effectiveness of Avastin in GBM is based on tumor response. 

Avastin is designed to directly bind to VEGF extracellularly to prevent interaction with 

VEGF receptors (VEGFR) on the surface of endothelial cells, thereby inhibiting its biologic

activity.VEGFR is the family of receptors primarily responsible for pro-angiogenic VEGF 

signaling. Extracellular VEGF binding may provide specific inhibition of the VEGF pathway.

Reference:

http://www.avastin-hcp.com/mrcc/efficacy/role-of-VEGF

http://www.avastin.com/patient

ARESTIN®; exhibits synergistic effect with scaling and root planing (SRP) for periodontal disease.

ARESTIN® contains microspheres—tiny particles—that are smaller than grains of sand and are not visible to the eye. The microspheres are filled with the antibiotic minocycline hydrochloride. These microspheres release the antibiotic over time, killing bacteria so your gums can heal better than with SRP alone. 

Arestin makes SRP more effective in the treatment of periodontal disease.

Reference:

http://www.arestin.com/effectiveness/

                                                            -Good evening-

ARESTIN^® makes scaling and root
planing (SRP) more effective - See more at: http://www.arestin.com/effectiveness/#sthash.cLr62blg.dpuf

FDA Approves Abraxane Drug for Pancreatic Cancer

ABRAXANE® for Injectable Suspension: (paclitaxel protein-bound particles) for Injectable Suspension.

The albumin serves as a delivery vehicle, improving the transportation of the drug to the target cancer sites.The Food and Drug Administration (FDA) has recently approved the use of Abraxane in those patients suffering from end-stage pancreatic cancer. Based upon clinical trials, the novel drug should help to extend life expectancy and, hopefully, provide a better quality of life.

Paclitaxel is one of several cytoskeletal drugs hat target tubulin. Paclitaxel-treated cells have defects in mitotic spindle assembly, chromosome segregation, and cell division. Unlike other tubulin-targeting drugs that inhibit microtubule assembly, paclitaxel stabilizes the microtubule polymer and protects it from disassembly. Chromosomes are thus unable to achieve a metaphase spindle configuration. This blocks progression of mitosis, and prolonged activation of the mitotic checkpoint triggers apoptosis or reversion to the G-phase of the cell cycle without cell division.

DOXIL (doxorubicin hcl liposome injection)

DOXIL (doxorubicin hcl liposome injection) is doxorubicin HCl encapsulated in long-circulating STEALTH® liposomes. Liposomes are microscopic vesicles composed of a phospholipid bilayer that are capable of encapsulating active drugs. The STEALTH® liposomes of DOXIL (doxorubicin hcl liposome injection) are formulated with surface-bound methoxypolyethylene glycol (MPEG), a process often referred to as pegylation, to protect liposomes from detection by the mononuclear phagocyte system (MPS) and to increase blood circulation time.

It is an anthracyclic antibiotic, closely related to the daunomycin, and like all anthracyclines, it works by intercalating DNA, with the most serious adverse effect being life-threatening heart damage. It is commonly used in the treatment of a wide range of cancers, including hematological malignancies, many types of carcinoma, and soft tissue sarcomas.

Molecular mechanism:

1. Doxorubicin helps to stabilize complexes containing double-stranded DNA and the enzyme topoisomerase II: this enzyme then cuts both of the DNA strands, which leads to the death of both normal cells (predominantly via topoisomerase IIβ) and in tumour cells that are susceptible to the drug (predominantly via topoisomerase IIα), thus accounting for both the toxicity and anti-tumour efficacy of doxorubicin.

2. Doxorubicin increases the production of ceramides inside cells, which leads to the latent transcription factor CREB3L1 translocating from the endoplasmic reticulum to the Golgi apparatus. Two proteases (S1P and S2P) then cut the CREB3L1 protein; and its amino-terminal fragment then migrates into the nucleus, where it acts as a transcription factor to activate the CDNK1A locus and additional genes. This leads to increased expression of the p21 protein along with other proteins that inhibit the proliferation of tumour cells.

Reference:
1. http://elife.elifesciences.org/content/1/e00387
2. http://www.rxlist.com/doxil-drug/clinical-pharmacology.htm
3. www.doxil.com

IMATINIB in Chronic myeloid leukemia

 

 


Reference:
www.gleevec.com

                                                                    Good day:-)

Cancer stem cells; novel target for cancer treatment

Cancer stem cells are an underlying cause of tumor recurrence and metastasis. The majority of cancer drugs, while killing the bulk of tumor cells, ultimately fail to induce durable clinical responses because these cells develop a resistance to treatment over time. A reason for this acquired resistance may be the presence of small minority of cells in the tumor called cancer stem cells (CSC). These CSCs are often resistant to existing cancer therapies including targeted drugs, chemo- and radiation therapy.

The ability of CSCs to move to other sites in the body, combined with the capability to initiate a new tumor mass, may implicate CSCs as an important factor in the formation of metastases. Metastatic tumor sites are the cause of death in more than 90% of human cancer patients. Cancer stems cells have been found in many types of tumors, including leukemia, myeloma, breast, prostate, colon, brain, lung and other cancer. 

In order to develop truly effective treatments that can create a durable clinical response it is important to develop drugs that can target and kill CSCs. A major factor that has prevented the discovery of drugs targeting CSCs is that isolated CSCs rapidly differentiate in culture, yielding the non-CSCs that represent the majority of cells in tumors.

Reference

1. http://www.verastem.com/research/

''Innovation distinguishes between a leader and a follower'' ; STEVE JOBS

mechanism of soliris