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Friday, February 21, 2014

Chemical kinetics

Chemical kinetics

Reaction rate tends to increase with concentration – a phenomenon explained by collision theory.
Chemical kinetics, also known as reaction kinetics, is the study of rates of chemical processes. Chemical kinetics includes investigations of how different experimental conditions can influence the speed of a chemical reaction and yield information about the reaction's mechanism and transition states, as well as the construction of mathematical models that can describe the characteristics of a chemical reaction. In 1864, Peter Waage and Cato Guldberg pioneered the development of chemical kinetics by formulating the law of mass action, which states that the speed of a chemical reaction is proportional to the quantity of the reacting substances.
Chemical kinetics deals with the experimental determination of reaction rates from which rate laws and rate constants are derived. Relatively simple rate laws exist for zero-order reactions (for which reaction rates are independent of concentration), first-order reactions, and second-order reactions, and can be derived for others. In consecutive reactions, the rate-determining step often determines the kinetics. In consecutive first-order reactions, a steady state approximation can simplify the rate law. The activation energy for a reaction is experimentally determined through the Arrhenius equation and the Eyring equation. The main factors that influence the reaction rate include: the physical state of the reactants, the concentrations of the reactants, the temperature at which the reaction occurs, and whether or not any catalysts are present in the reaction.

Factors affecting reaction rate

Nature of the reactants

Depending upon what substances are reacting, the reaction rate varies. Acid/base reactions, the formation of salts, and ion exchange are fast reactions. When covalent bond formation takes place between the molecules and when large molecules are formed, the reactions tend to be very slow. Nature and strength of bonds in reactant molecules greatly influence the rate of its transformation into products.

Physical state

The physical state (solid, liquid, or gas) of a reactant is also an important factor of the rate of change. When reactants are in the same phase, as in aqueous solution, thermal motion brings them into contact. However, when they are in different phases, the reaction is limited to the interface between the reactants. Reaction can occur only at their area of contact; in the case of a liquid and a gas, at the surface of the liquid. Vigorous shaking and stirring may be needed to bring the reaction to completion. This means that the more finely divided a solid or liquid reactant the greater its surface area per unit volume and the more contact it makes with the other reactant, thus the faster the reaction. To make an analogy, for example, when one starts a fire, one uses wood chips and small branches — one does not start with large logs right away. In organic chemistry, on water reactions are the exception to the rule that homogeneous reactions take place faster than heterogeneous reactions.


The reactions are due to collisions of reactant species. The frequency with which the molecules or ions collide depends upon their concentrations. The more crowded the molecules are, the more likely they are to collide and react with one another. Thus, an increase in the concentrations of the reactants will result in the corresponding increase in the reaction rate, while a decrease in the concentrations will have a reverse effect. For example, combustion that occurs in air (21% oxygen) will occur more rapidly in pure oxygen.


Temperature usually has a major effect on the rate of a chemical reaction. Molecules at a higher temperature have more thermal energy. Although collision frequency is greater at higher temperatures, this alone contributes only a very small proportion to the increase in rate of reaction. Much more important is the fact that the proportion of reactant molecules with sufficient energy to react (energy greater than activation energy: E > Ea) is significantly higher and is explained in detail by the Maxwell–Boltzmann distribution of molecular energies.
The 'rule of thumb' that the rate of chemical reactions doubles for every 10 °C temperature rise is a common misconception. This may have been generalized from the special case of biological systems, where the α (temperature coefficient) is often between 1.5 and 2.5.
A reaction's kinetics can also be studied with a temperature jump approach. This involves using a sharp rise in temperature and observing the relaxation time of the return to equilibrium. A particularly useful form of temperature jump apparatus is a shock tube, which can rapidly jump a gas's temperature by more than 1000 degrees.


Generic potential energy diagram showing the effect of a catalyst in a hypothetical endothermic chemical reaction. The presence of the catalyst opens a different reaction pathway (shown in red) with a lower activation energy. The final result and the overall thermodynamics are the same.
A catalyst is a substance that accelerates the rate of a chemical reaction but remains chemically unchanged afterwards. The catalyst increases rate reaction by providing a different reaction mechanism to occur with a lower activation energy. In autocatalysis a reaction product is itself a catalyst for that reaction leading to positive feedback. Proteins that act as catalysts in biochemical reactions are called enzymes. Michaelis–Menten kinetics describe the rate of enzyme mediated reactions. A catalyst does not affect the position of the equilibria, as the catalyst speeds up the backward and forward reactions equally.
In certain organic molecules, specific substituents can have an influence on reaction rate in neighbouring group participation.
Agitating or mixing a solution will also accelerate the rate of a chemical reaction, as this gives the particles greater kinetic energy, increasing the number of collisions between reactants and, therefore, the possibility of successful collisions.


Increasing the pressure in a gaseous reaction will increase the number of collisions between reactants, increasing the rate of reaction. This is because the activity of a gas is directly proportional to the partial pressure of the gas. This is similar to the effect of increasing the concentration of a solution.
In addition to this straightforward mass-action effect, the rate coefficients themselves can change due to pressure. The rate coefficients and products of many high-temperature gas-phase reactions change if an inert gas is added to the mixture; variations on this effect are called fall-off and chemical activation. These phenomena are due to exothermic or endothermic reactions occurring faster than heat transfer, causing the reacting molecules to have non-thermal energy distributions (non-Boltzmann distribution). Increasing the pressure increases the heat transfer rate between the reacting molecules and the rest of the system, reducing this effect.
Condensed-phase rate coefficients can also be affected by (very high) pressure; this is a completely different effect than fall-off or chemical-activation. It is often studied using diamond anvils.
A reaction's kinetics can also be studied with a pressure jump approach. This involves making fast changes in pressure and observing the relaxation time of the return to equilibrium.


While a chemical kinetics is concerned with the rate of a chemical reaction, thermodynamics determines the extent to which reactions occur. In a reversible reaction, chemical equilibrium is reached when the rates of the forward and reverse reactions are equal (the principle of detailed balance) and the concentrations of the reactants and products no longer change. This is demonstrated by, for example, the Haber–Bosch process for combining nitrogen and hydrogen to produce ammonia. Chemical clock reactions such as the Belousov–Zhabotinsky reaction demonstrate that component concentrations can oscillate for a long time before finally attaining the equilibrium.

Free energy

In general terms, the free energy change (ΔG) of a reaction determines whether a chemical change will take place, but kinetics describes how fast the reaction is. A reaction can be very exothermic and have a very positive entropy change but will not happen in practice if the reaction is too slow. If a reactant can produce two different products, the thermodynamically most stable one will in general form, except in special circumstances when the reaction is said to be under kinetic reaction control. The Curtin–Hammett principle applies when determining the product ratio for two reactants interconverting rapidly, each going to a different product. It is possible to make predictions about reaction rate constants for a reaction from free-energy relationships.
The kinetic isotope effect is the difference in the rate of a chemical reaction when an atom in one of the reactants is replaced by one of its isotopes.
Chemical kinetics provides information on residence time and heat transfer in a chemical reactor in chemical engineering and the molar mass distribution in polymer chemistry.


The mathematical models that describe chemical reaction kinetics provide chemists and chemical engineers with tools to better understand and describe chemical processes such as food decomposition, microorganism growth, stratospheric ozone decomposition, and the complex chemistry of biological systems. These models can also be used in the design or modification of chemical reactors to optimize product yield, more efficiently separate products, and eliminate environmentally harmful by-products. When performing catalytic cracking of heavy hydrocarbons into gasoline and light gas, for example, kinetic models can be used to find the temperature and pressure at which the highest yield of heavy hydrocarbons into gasoline will occur. Kinetics is also a basic aspect of chemistry.

See also


  • Preparing for the Chemistry AP Exam. Upper Saddle River, New Jersey: Pearson Education, 2004. 131–134. ISBN 0-536-73157-8

Electron pair

Electron pair

                                                                             By Miss Sejal D Jethva

In chemistry, an electron pair or a Lewis pair consists of two electrons that occupy the same orbital but have opposite spins. The electron pair concept was introduced in a 1916 paper of Gilbert N. Lewis.[1]
MO diagrams depicting covalent (left) and polar covalent (right) bonding in a diatomic molecule. In both cases a bond is created by the formation of an electron pair.
Because electrons are fermions, the Pauli exclusion principle forbids these particles from having exactly the same quantum numbers. Therefore the only way to occupy the same orbital, i.e. have the same orbital quantum numbers, is to differ in the spin quantum number. This limits the number of electrons in the same orbital to exactly two.
The pairing of spins is often energetically favorable and electron pairs therefore play a very large role in chemistry. They can form
  1. a chemical bond between two atoms
  2. as a lone pair.
  3. fill the core levels of an atom.
Because the spins are paired, the magnetic moment of the electrons cancels and the contribution of the pair to the magnetic properties will in general be a diamagnetic one.
Although a strong tendency to pair off electrons can be observed in chemistry, it is also possible that electrons occur as unpaired electrons.
In the case of metallic bonding the magnetic moments also compensate to a large extent, but the bonding is more communal so that individual pairs of electrons cannot be distinguished and it is better to consider the electrons as a collective 'ocean'.
A very special case of electron pair formation occurs in superconductivity: the formation of Cooper pairs.

Alkylating antineoplastic agent By Dr.Rajarshi N Patel & Mr.Dharam M Pandya

Alkylating antineoplastic agent

                                         Dr.Rajarshi N Patel & Mr.Dharam M Pandya

An alkylating antineoplastic agent is an alkylating agent used in cancer treatment that attaches an alkyl group (CnH2n+1) to DNA.[1]
The alkyl group is attached to the guanine base of DNA, at the number 7 nitrogen atom of the purine ring.
Since cancer cells, in general, proliferate faster and with less error-correcting than healthy cells, cancer cells are more sensitive to DNA damage — such as being alkylated. Alkylating agents are used to treat several cancers. However, they are also toxic to normal cells (cytotoxic), leading to damage, in particular in cells that divide frequently, as those in the gastrointestinal tract, bone marrow, testicles and ovaries, which can cause loss of fertility. Most of the alkylating agents are also carcinogenic. Hyperthermia is especially effective at enhancing the effects of alkylating agents.[2]


Before their use in chemotherapy, alkylating agents were better known for their use as sulfur mustard, ("mustard gas") and related chemical weapons in World War I. The nitrogen mustards were the first alkylating agents used medically, as well as the first modern cancer chemotherapies. Goodman, Gilman, and others at Yale began studying nitrogen mustards at Yale in 1942, and, following the sometimes dramatic but highly variable responses of experimental tumors in mice to treatment, these agents were first tested in humans late that year. Use of methyl bis (B-chloroethyl)emine hydrochloride (mechlorethamine, mustine) and tris (B-chloroethy) amine hydrochloride for Hodgkin's disease lymphosarcoma, leukemia, and other malignancies resulted in striking but temporary dissolution of tumor masses. Because of secrecy surrounding the war gas program, these results were not published until 1946.[3] These publications spurred rapid advancement in the previously non-existent field of cancer chemotherapy, and a wealth of new alkylating agents with therapeutic effect were discovered over the following two decades.[4]
A common myth holds that Goodman and Gilman were prompted to study nitrogen mustards as a potential treatment for cancer following a 1943 incident in Bari, Italy, where survivors exposed to mustard gas became leukopenic. In fact, animal and human trials had begun the previous year, Gilman makes no mention of such an episode in his recounting of the early trials of nitrogen mustards,[5] and the marrow suppressing effects of mustard gas had been known since the close of World War I.[4]

Agents acting nonspecifically

Some alkylating agents are active under conditions present in cells; and the same mechanism that makes them toxic allows them to be used as anti-cancer drugs. They stop tumor growth by crosslinking guanine nucleobases in DNA double-helix strands, directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. These drugs act nonspecifically.

Agents requiring activation

Some of the substances require conversion into active substances in vivo (e.g., cyclophosphamide).
Cyclophosphamide is one of the most potent immunosuppressive substances. In small dosages, it is very efficient in the therapy of systemic lupus erythematosus, autoimmune hemolytic anemias, Wegener's granulomatosis, and other autoimmune diseases. High dosages cause pancytopenia and hemorrhagic cystitis.

Dialkylating agents, limpet attachment, and monoalkylating agents

Dialkylating agents can react with two different 7-N-guanine residues, and, if these are in different strands of DNA, the result is cross-linkage of the DNA strands, which prevents uncoiling of the DNA double helix. If the two guanine residues are in the same strand, the result is called limpet attachment of the drug molecule to the DNA. Busulfan is an example of a dialkylating agent: it is the methanesulfonate diester of 1,4-butanediol. Methanesulfonate can be eliminated as a leaving group. Both ends of the molecule can be attacked by DNA bases, producing a butylene crosslink between two different bases.
Monoalkylating agents can react only with one 7-N of guanine.
Limpet attachment and monoalkylation do not prevent the separation of the two DNA strands of the double helix but do prevent vital DNA-processing enzymes from accessing the DNA. The final result is inhibition of cell growth or stimulation of apoptosis, cell suicide.


In the Anatomical Therapeutic Chemical Classification System, alkylating agents are classified under L01A.

Classical alkylating agents

Many of the agents are known as "Classical alkylating agents". These include true alkyl groups, and have been known for a longer time than some of the other alkylating agents. Examples include melphalan and chlorambucil.[6]
They destroy proliferating cancer cells by adding an alkyl group to DNA molecule and preventing its replication.
The following three groups are almost always considered "classical".
Thiotepa and its analogues are usually considered classical, but can be considered nonclassical.


Platinum-based chemotherapeutic drugs (termed platinum analogues) act in a similar manner. These agents do not have an alkyl group, but nevertheless damage DNA.[8] They permanently coordinate to DNA to interfere with DNA repair, so they are sometimes described as "alkylating-like".
These agents also bind at N7 of guanine.


Certain alkylating agents are sometimes described as "nonclassical". There is not a perfect consensus on which items are included in this category, but, in general, they include:
  • The platinum agents are also sometimes described as nonclassical.[14]


Alkylating antineoplastic agents have limitations. Their functionality has been found to be limited when in the presence of the DNA-repair enzyme O-6-methylguanine-DNA methyltransferase (MGMT). Cross-linking of double-stranded DNA by alkylating agents is inhibited by the cellular DNA-repair mechanism, MGMT. If the MGMT promoter region is methylated, the cells no longer produce MGMT, and are therefore more responsive to alkylating agents. Methylation of the MGMT promoter in gliomas is a useful predictor of the responsiveness of tumors to alkylating agents.[15]


  1. Jump up ^ "antineop". Archived from the original on 7 March 2009. Retrieved 2009-01-24.
  2. Jump up ^ Wiedemann GJ, Robins HI, Gutsche S, Mentzel M, Deeken M, Katschinski DM, Eleftheriadis S, Crahé R, Weiss C, Storer B, Wagner T. (May 1996). "Ifosfamide, carboplatin and etoposide (ICE) combined with 41.8 degrees C whole body hyperthermia in patients with refractory sarcoma". European Journal of Cancer 32A (5): 888–92. PMID 9081372.
  3. Jump up ^ Goodman LS, Wintrobe MM, Dameshek W, Goodman MJ, Gilman AZ, McLennan MT (1946). "Nitrogen mustard therapy". JAMA 132 (3): 126–132. doi:10.1001/jama.1946.02870380008004.
  4. ^ Jump up to: a b Scott RB (1970). "Cancer chemotherapy--the first twenty-five years". Br Med J. 4 (5730): 259–265. doi:10.1136/bmj.4.5730.259. PMC 1819834. PMID 4319950.
  5. Jump up ^ Gilman A (1963). "The initial clinical trial of nitrogen mustard". Am J Surg. 105 (5): 574–8. doi:10.1016/0002-9610(63)90232-0. PMID 13947966.
  6. Jump up ^ McClean S, Costelloe C, Denny WA, Searcey M, Wakelin LP (June 1999). "Sequence selectivity, cross-linking efficiency and cytotoxicity of DNA-targeted 4-anilinoquinoline aniline mustards". Anticancer Drug Des. 14 (3): 187–204. PMID 10500495.
  7. ^ Jump up to: a b Takimoto CH, Calvo E. "Principles of Oncologic Pharmacotherapy" in Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (Eds) Cancer Management: A Multidisciplinary Approach. 11 ed. 2008.
  8. Jump up ^ Cruet-Hennequart S, Glynn MT, Murillo LS, Coyne S, Carty MP (April 2008). "Enhanced DNA-PK-mediated RPA2 hyperphosphorylation in DNA polymerase eta-deficient human cells treated with cisplatin and oxaliplatin". DNA Repair (Amst.) 7 (4): 582–96. doi:10.1016/j.dnarep.2007.12.012. PMID 18289945.
  9. Jump up ^ Armand JP, Ribrag V, Harrousseau JL, Abrey L (June 2007). "Reappraisal of the use of procarbazine in the treatment of lymphomas and brain tumors". Ther Clin Risk Manag 3 (2): 213–24. doi:10.2147/tcrm.2007.3.2.213. PMC 1936303. PMID 18360630.
  10. Jump up ^ Yasko, Joyce M.; Kirkwood, John M.; Lotze, Michael T. (1998). Current cancer therapeutics. Edinburgh: Churchill Livingstone. p. 3. ISBN 0-443-06527-6.
  11. Jump up ^ Schmit-Neuerburg, Klaus-Peter; Reiner Labitzke (2000). Manual of Cable Osteosyntheses: History, Technical Basis, Biomechanics of the Tension Band Principle, and Instructions for Operation. Berlin: Springer. p. 166. ISBN 3-540-66508-0.
  12. Jump up ^ Bailey, Christopher J.; Corner, Jessica (2001). Cancer nursing: care in context. Oxford: Blackwell Science. p. 214. ISBN 0-632-03998-1.
  13. Jump up ^ Kutner, Jean S; Gonzales, Ralph (2006). Current Practice Guidelines in Primary Care: 2007 (Current Practice Guidelines in Primary Care). McGraw-Hill Professional. p. 118. ISBN 0-07-147781-0.
  14. Jump up ^ Pizzo, Philip A.; Poplack, David G. (2006). Principles and practice of pediatric oncology. Hagerstown, MD: Lippincott Williams & Wilkins. p. 313. ISBN 0-7817-5492-5.
  15. Jump up ^ N Engl J Med 2000;343;1350-4.

Friday, March 8, 2013

Clinical Trials

Clinical Trials: Medical clinical trials plays an important role in development of new drugs. These trials are conducted in three phases. Introduction Clinical trials are a means of developing new treatments and medications for diseases and conditions. There are strict rules for clinical trials, which are monitored by the National Institutes of Health and the U.S Food and Drug Administration. Clinical trials are also called clinical studies, research protocols or medical research and often compare one drug against another to see which is more effective, or the medicine or procedure in a specific demographic group or for a specific disease. About Clinical Trials Why Participate in a Clinical Trial? Participants in clinical trials can play a more active role in their health care, gain access to new research treatments before they are widely available and help others by contributing to medical research. Where Do the Ideas for Trials Come from? Ideas for clinical trials usually come from researchers. After researchers test new therapies or procedures in the laboratory and/or in animal studies, the treatments with the most promising test results are moved into clinical trials. During a trial, more and more information is gained about a new treatment, its risks and how well it may or may not work. Who Sponsors Clinical Trials? Clinical trials are sponsored or funded by a variety of organizations or individuals such as physicians, medical institutions,foundations, voluntary medical-related groups and pharmaceutical companies, in addition to federal agencies such as the National Institutes of Health, the Department of Defense and the Department of Veteran’s Affairs. Trials can take place in a variety of locations, such as hospitals, universities, doctors’ offices or community clinics. What is a Protocol? A protocol is a study plan on which all clinical trials are based. The plan is carefully designed to safeguard the health of the participants as well as answer specific research questions. A protocol describes what types of people can participate in the trial; the schedule of tests, procedures, medications and dosages; and the length of the study. While in clinical trial, participants following a protocol are seen regularly by the research staff to monitor their health and to determine the safety and effectiveness of their treatment. What is a Placebo? A placebo is an inactive pill, liquid, or powder that has no treatment value. In clinical trials, experimental treatments are often compared with placebos to assess the treatment’s effectiveness. In some studies, the participants in the control group will receive a placebo instead of an active drug or treatment. What is a Control or Control Group? A control is the standard by which experimental observations are evaluated. In many clinical trials, one group of patients will be given an experimental drug or treatment, while the control group is given either a standard treatment for the illness or a placebo. What are the Different Types of Clinical Trials? Treatment trials test new treatments, new combinations of drugs, or new approaches to surgery or radiation therapy. Prevention trials look for better ways to prevent disease in people who have never had the disease or to prevent a disease from returning. These approaches may include medicine, vitamins, vaccines, minerals or lifestyle changes. Screening trials test the best way to detect certain diseases or health conditions. Quality of Life trials (or Supportive Caretrials) explore ways to improve comfort and the equality of life for individuals with a chronic illness. Classification of Clinical Trials There are three types of clinical trials – phase I, phase II and phase III – each one is designed to learn something different about a new medical treatment. Phase I Trials A phase I trial is the first test of a new treatment, and it uses the fewest number of patients (20-30 patients is typical). A phase I trial for a new drug is designed to determine the safety of the new drug, how to best administer it and the correct dosage (i.e., one that will minimize undesirable side effects). Because investigators are very interested in how the drug behaves in the body, patients in a phase I trial undergo frequent monitoring of their vital signs. Although drugs being tested in a phase I trial have shown promise in the laboratory, there is no guarantee that the drug will have any positive effects on a patient. Patients participating in a phase I drug trial help advance basic medical knowledge; they may or may not reap any personal benefits. Phase II Trials After a phase I clinical trial has determined the safe dose of a drug, it can enter a phase II trial, which begins the process of determining the drug’s effectiveness in treating a specific type of disease. Because a phase II trial involves more patients than a phase I trial, physicians also have a chance to observe any less common side effects associated with the drug. In a phase II trial, which can involve 100 patients or more, physicians carefully monitor patients for a drug effect. For example, in a clinical trial testing a drug to increase the number of platelets in the blood, patients would have frequent blood samples taken, but they might also undergo several physical exams and other tests. The high level of patient monitoring in a phase II trial can be very time-consuming, so patients should take this into account when considering a phase II trial.

Monday, February 4, 2013


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Sunday, August 12, 2012

Ion exchange resin and its application in pharmaceutical dosage forms, and drug delivery systems.

Ion exchange resins are cross linked polymers of polystyrene, up on which a negatively charged or a positively charged functional group can be added to get an anion exchange resin (Resin- )or a cation exchange resin Resin +(Resin + Or Resin- ). When these resins are mixed with drug molecule which has a negative charge in its one or more functional group as a result of polarity, or as in salt form, or as a result of resonance, such a drug can form a complex with a resin as follow.

1.) Resin + Drug-
2.) Resin- Drug+

*The resulting resin drug complex stability depends on how strong are the acidic or basic functional groups on resin, stronger functional group result in to formation of very stable resin drug complex, and vice a versa , both has its applications in sustained release drug delivery systems, a resin with strong acidic or basic functional group tend to provide a much more delayed drug release, where drug release is bit faster with weak acidic and basic functional group resins.

When Resin- Drug+ or Resin + Drug- complex (drug resinate ) comes in contact with acid(in stomach) or base(in intestine), it start releasing drug molecule in exchange of similar charged ion for example if drug molecule is positively charged, then it is released from Resin- Drug+ complex when it come in contact with Hydrogen Ion( H+) , similarly a Resin + Drug- or basic drug resin complex will start releasing drug when it comes in contact with basic ions ( in intestine ) OH – NH3- .
Release of drug molecule from Resin +Drug complex takes place due to higher concentration of replacing ions (H+ , or OH – NH3- ).

Masking Taste of drug with ion exchange resin:
There are some drugs which are very bitter in taste like Bromhexin and Quinine, patients has very low acceptability for such drugs some time patients vomit and expelling all of the consumed dose which may result in to dosing error, therefore when such drugs are formulated with ion exchange resins which binds such drugs they do not release drug on taste buds over tongue as a result taste of drug is masked, and when it come in contact with gastric acid bromhexin is released in to gut.

Sustained-release drug delivery system:
Ion exchange resins may not alone give capability to formulate it in to a sustained release dosage form , to make it a good sustained release drug delivery system , proper selection of resin is important a resin with strong acidic or basic functional group provides strong complexation with drug therefore are good candidates for delayed drug release, likewise when early release is intended a weaker acidic or basic functional group resins are useful . Drug resinate is also required to be coated with semipermiable film forming polymers, as drug resinate complex can not be solely relied up on for the intended use. ( ethylcellulose ). In order to maintained the sustained release property of ion exchange resin drug complex it is pretreated with polyethylene glycol so that it do not swell and break open the film coating when it come in contact with gastric juice.

Ion exchange resins are required to be washed with, suitable organic solvent, to remove residual organic or chemical impurities in ion exchange resin, followed by washing with purified water, and regeneration if required, before using for actual process. Ion exchange resin are required to comply with requirements listed in 21 CFR 173.25 by US FDA.

Ion exchange resins have many other applications in pharmaceutical dosage form and drug delivery systems like , localized drug release, stabilization of drug molecule for chemical degradation .
Ion exchange resins are widely used in pharmaceutical industry for purification or raw water and in preparation of water for pharmaceutical use.

-Rajarshi Nareshkumar Patel

Novel Drugs: Cancer Chemotherapy Using Nanoparticles developed with Nanotechnology May Reduce Harmful Side Effects of Antineoplastic Agents.

Chemotherapy for cancer is most of the time associated with one or the other harmful side effect of antineoplastic drugs as these chemotherapeutic drugs themselves are very cytotoxic, i.e. they damage normal cells too.
Antineoplastic drugs bring about their anticancer action by inhibiting cancerour cells growth by virtue of alkylation of nucleotides in cancerous cells or by inhibition of folic acid uptake by cancerous cells or by inhibiting cell division by binding with tubulin and microtubulin in a cancerous cells, it is likely that these drug are also absorbed in to normal tissues, leading to untoward serious cytotoxic effects , like kidney damage and nerve damage in chemotherapy with cisplatin, a drug of choice in most of anticancer chemotherapies.

A new drug delivery technique is being studied which uses Nanotechnology to deliver a cytotoxic drugs specifically directly in to the cancer cells , such drug delivery technique will be able to provide an efficient cancer chemotherapy that do not have much side effects as they pose today , it was observed that with nanoparticle drug delivery system the concentration of drug required to kill the cancerous cell is lesser than required in conventional chemotherapy therapy. As the drug is absorbed efficiently in to targeted cells and also drug is protected from degradation in blood stream , certain class of the anticancerdrugs are very unstable and stay in plasma for a very little time, therefor to achieve the required effect a higher concentration of drug may be required to be administrated.

Nanotechnology drug delivery system involves placing an anticancer drug in to a tiny particles known as nanoparticles which recognize cancerous cells and deliver the drug only to cancerous cells , as nanoparticles are very minute particles (1 nm to 100 nanometer) , the dose of drug required to kill the cancerous cells were also found to be very low as compared to conventional therapy . As the required effective dose it self gets reduced than conventional therapy , the harmful effect of anticancer drug are also likely to be reduced.

A team of scientists from the Massachusetts Institute of Technology and Brigham and Women's Hospital conducted study. They stored an prodrug of cisplatin (which is used in most of cancer chemotherapies) within nanoparticles which they developed to target a specific protein in cancerous cells in prostate gland.
After these prodrug loaded nanoparticles were absorbed by cancerous cells the prodrug was released in to the cancerous cells and was converted in to an active form . The team demonstrated that these prodrug carrying nanoparticles were able to kill cancer cells in culture more efficiently than the drug alone.

Study was conducted by researchers, led by Dr. Omid Farokhzad and Dr. Stephen Lippard, to study nanoparticle drug delivery system for an effective and safer option for chemotherapy in living animals. Their research work is published in Proceedings of the National Academy of Sciences, in Jan 2011 issue of the journal, the study was funded in part by NIH’s National Cancer Institute (NCI) and National Institute for Biomedical Imaging and Bioengineering (NIBIB).

By applying this drug delivery by nanoparticles they were able to shrink tumors in mice with smaller doses of the drug to reduce harmful side effects. Only 30% of the dose of prodrug of cisplatin was required to diminish the tumor by using the drug carrying nanoparticles, than that of standard dose of cisplatin as such.
Researchers initially studied different doses of nanoparticle bound drug in rats and mice, both the types of animals maintained their body weight and survived at higher doses of the drug when drug was delivered using nanoparticles than when injected without nanoparticles. It was also found that the kidney damage was less in rats which received the nanoparticle bound drug.

Also it was found that binding nanoparticles provided greater stability of cisplatin prodrug in blood stream than that of injected alone , after one hour about 77 % of prodrug was found in blood stream when it was delivered using nanoparticles compared to only 16% available drug in case of drug delivered without nanoparticles, cispaltin is very unstable drug and remains in blood for very short time , which calls for more dose to get the desired effect.

Rajarshi Patel