Chemotherapeutic agents

Summary

This video script offers an insightful overview of chemotherapeutic agents used in cancer treatment. It covers various drug classes, including alkala agents, antimetabolites, microtubular targeting agents, topoisomerase inhibitors, anthracyclines, and monoclonal antibodies. Each class's mechanism of action and side effects are discussed, providing a comprehensive understanding of how these agents target cancer cells while minimizing harm to healthy cells.

Takeaways

• 🔬 Chemotherapeutic agents are drugs used to treat cancer by interfering with the ability of cancer cells to grow and divide.
• 🌿 Vinca alkaloids and taxanes are two classes of chemotherapeutic agents that affect microtubules, leading to cell death by disrupting cell division.
• 🔄 Topoisomerase inhibitors, such as Topo I and Topo II, prevent the relaxation of supercoiled DNA, leading to cell death by inhibiting DNA replication.
• 🧪 Alkylating agents, including both typical and atypical agents like platinum compounds, work by attaching to DNA, causing cross-linking and preventing replication.
• 💊 Antimetabolites mimic normal cell compounds to inhibit DNA replication, with specific action during the S phase of the cell cycle.
• 🌐 Microtubule targeting agents, like vinca alkaloids and taxanes, either destroy or stabilize microtubules, preventing their function and halting cell division.
• 🩺 Monoclonal antibodies are engineered to target specific proteins or receptors on cancer cells, offering a more targeted approach to cancer treatment.
• 💉 Anthracyclines have a complex mechanism of action, including intercalating DNA, inhibiting topoisomerase II, and generating reactive oxygen species.
• 🩹 Side effects of chemotherapeutic agents can be severe, including myelosuppression, neuropathy, and organ toxicity, and vary depending on the class of the drug.
• 🧬 Hormonal therapies, such as anti-estrogens for breast cancer and anti-androgens for prostate cancer, aim to block hormone production or activity to inhibit cancer growth.

Q & A

What are the two classes of chemotherapeutic agents that affect microtubules?

The two classes of chemotherapeutic agents that affect microtubules are Vinca alkaloids and Taxanes.

How do Alkylating agents damage DNA?

Alkylating agents damage DNA by attaching alkyl groups to DNA, usually between two base pairs, allowing for cross-linking of base pairs, which damages the DNA and makes it unable to replicate, leading to cell death.

What are the side effects commonly associated with Alkylating agents?

Common side effects of Alkylating agents include myelosuppression, nausea and vomiting, secondary malignancies, infertility, and hemorrhagic cystitis.

Which chemotherapeutic agent is known to be the strongest inducer of nausea and vomiting?

Cisplatin is known to be the strongest inducer of nausea and vomiting among the chemotherapeutic agents discussed.

How do antimetabolites inhibit DNA replication?

Antimetabolites inhibit DNA replication by mimicking normal cell compounds, thereby interfering with the normal process of DNA replication.

What are the three categories of antimetabolites mentioned in the script?

The three categories of antimetabolites mentioned are folate inhibitors, pyrimidine inhibitors, and purine analogs.

What is the primary side effect of Methotrexate, a folate inhibitor?

The primary side effect of Methotrexate is mucositis, along with myelosuppression.

How do microtubular targeting agents like Vinca alkaloids and Taxanes affect cancer cells?

Vinca alkaloids destroy microtubules, preventing their function, while Taxanes stabilize microtubules, both rendering them useless and inhibiting mitosis.

What are the side effects associated with Topoisomerase inhibitors?

Side effects associated with Topoisomerase inhibitors include myelosuppression, mucositis, and secondary malignancies such as acute myeloid leukemia.

What is the mechanism of action of Anthracyclines?

Anthracyclines have an ambiguous mechanism of action; they can intercalate DNA, inhibit topoisomerase II, generate reactive oxygen species, and cause alkylation.

What are the side effects of administering Anthracyclines?

Side effects of administering Anthracyclines include an increased risk of biventricular heart failure based on cumulative dose and tissue necrosis in case of extravasation.

Outlines

00:00

🔬 Chemotherapeutic Agents Overview

The script introduces various chemotherapeutic agents used in cancer treatment, focusing on their mechanisms of action and side effects. It discusses three main classes of drugs: alkala agents, antimetabolites, and microtubular targeting agents. Alkala agents, such as cyclophosphamide and cisplatin, work by attaching to DNA and causing cross-linking, which damages the DNA and leads to cell death. Antimetabolites inhibit DNA replication by mimicking normal cell compounds and are specific to cells in the S phase of the cell cycle. Microtubular targeting agents, like vinka alkaloids and taxanes, affect the mitotic spindle, preventing cell division. The script also mentions the importance of these agents being more effective at killing cancer cells than normal cells.

05:02

💊 Side Effects and Specific Agents

This section delves into the side effects associated with chemotherapeutic agents, such as myelosuppression, nausea, vomiting, and neuropathy. It also highlights specific agents within each class, including typical and atypical alkala agents, and their unique side effects. For instance, cisplatin is noted for its strong induction of nausea and vomiting, while atypical alkala agents like nitrosoureas can cause pulmonary toxicity and central nervous system problems. The script emphasizes the need for careful administration and the management of these side effects in cancer treatment.

10:02

🧬 DNA Interaction and Topoisomerase Inhibitors

The script explains how anthracyclines interact with DNA, potentially intercalating between strands, inhibiting topoisomerase 2, generating reactive oxygen species, and causing cross-linking between DNA base pairs. It also discusses topoisomerase inhibitors, which prevent the relaxation or recoiling of supercoiled DNA, leading to cell death. Specific drugs like topotecan and irinotecan are mentioned, along with their side effects, which include myelosuppression and diarrhea. The section also touches on the use of these drugs in combination regimens, such as the 7+3 chemotherapy plan.

15:03

🏥 Monoclonal Antibodies and Other Therapies

The final paragraph discusses monoclonal antibodies, which are synthesized to target specific receptors or factors that inhibit cancer growth. The script explains the origin of these antibodies based on their suffixes, indicating whether they are derived from mice, chimeric, humanized, or fully human. Examples include rituximab, which targets CD20 for lymphoma treatment, and bevacizumab, which targets vascular endothelial growth factor for solid tumors. The script also briefly mentions other chemotherapeutic agents like bleomycin, which causes lung toxicity, and hormonal therapies for breast and prostate cancer. The summary concludes with a note on the importance of understanding the mechanisms of action and side effects of these agents in chemotherapy.

Keywords

💡Chemotherapeutic Agents

Chemotherapeutic agents are drugs used to treat cancer by interfering with the growth and spread of cancer cells. They can be classified into various groups based on their mechanisms of action. In the video, several classes of chemotherapeutic agents are discussed, including alkala agents, antimetabolites, microtubular targeting agents, topoisomerase inhibitors, anthracyclines, and monoclonal antibodies, each with distinct mechanisms and side effects.

💡Alka Agents

Alka agents are a class of chemotherapeutic drugs that attach alkal groups to DNA, causing cross-linking between base pairs and preventing DNA replication, ultimately leading to cell death. The video mentions both typical and atypical alkala agents, such as cyclophosphamide, cisplatin, and the nitrosoureas, which have different side effects like myelosuppression, nephrotoxicity, and pulmonary toxicity.

💡Antimetabolites

Antimetabolites are a group of chemotherapeutic agents that inhibit DNA replication by mimicking normal cell compounds. They are specific to cells in the S phase of the cell cycle. Examples from the video include folate inhibitors like methotrexate, pyrimidine inhibitors like 5-fluorouracil, and purine analogs like 6-mercaptopurine, each with unique side effects such as mucositis and myelosuppression.

💡Microtubular Targeting Agents

Microtubular targeting agents interfere with the normal function of microtubules during cell division, leading to cell death. Vinca alkaloids, such as vincristine, destroy microtubules, while taxanes, like paclitaxel and docetaxel, stabilize them. Both actions prevent the microtubules from separating chromosomes, which is crucial for cell division. Side effects of these agents include peripheral neuropathy and myelosuppression.

💡Topoisomerase Inhibitors

Topoisomerase inhibitors are drugs that target enzymes called topoisomerases, which are involved in DNA replication and transcription. There are two types discussed in the video: topoisomerase I inhibitors, like topotecan and irinotecan, which prevent the relaxation of supercoiled DNA, and topoisomerase II inhibitors, like etoposide and teniposide, which inhibit the re-ligation of DNA strands after transcription. Side effects include myelosuppression and, in the case of irinotecan, severe diarrhea.

💡Anthracyclines

Anthracyclines are a class of antibiotics with a complex mechanism of action that includes intercalating DNA, inhibiting topoisomerase II, and generating reactive oxygen species. They are characterized by a 'rubisone' ending in their names, like doxorubicin. Side effects of anthracyclines include cardiotoxicity, which is dose-dependent, and the risk of extravasation injury if not administered properly.

💡Monoclonal Antibodies

Monoclonal antibodies are laboratory-produced molecules designed to target specific antigens on cancer cells. They can be derived from mice (omab), be chimeric (ximab), humanized (umab), or fully human (mumab). The video mentions several monoclonal antibodies, such as rituximab for B-cell lymphomas, trastuzumab for HER2-positive breast cancer, and bevacizumab for solid tumors, each with different side effects like hypersensitivity reactions and GI perforations.

💡Myelosuppression

Myelosuppression refers to the decrease in the production of blood cells in the bone marrow, often a side effect of chemotherapy. It can lead to anemia, neutropenia, and thrombocytopenia, increasing the risk of infections and bleeding. The video discusses myelosuppression as a common side effect of many chemotherapeutic agents, including alkala agents and antimetabolites.

💡Peripheral Neuropathy

Peripheral neuropathy is a type of nerve damage that affects the peripheral nervous system, causing symptoms like tingling, numbness, and pain in the hands and feet. It is a common side effect of certain chemotherapeutic agents, particularly microtubular targeting agents like vinca alkaloids and taxanes, as mentioned in the video.

💡Extravasation

Extravasation is the accidental leakage of a drug, especially a chemotherapeutic agent, into the surrounding tissue during administration. The video highlights the risk of anthracyclines causing tissue necrosis if they extravasate, which underscores the importance of careful administration by trained healthcare professionals.

💡Hormonal Therapies

Hormonal therapies are treatments that target hormone-sensitive cancers, such as breast and prostate cancers. The video discusses antiestrogens like tamoxifen for breast cancer and anti-androgens for prostate cancer, which work by blocking hormone production or action, thereby inhibiting cancer cell growth. These therapies can have specific side effects related to hormone imbalance.

Highlights

Vinka alkaloids and taxanes are chemotherapeutic agents that affect microtubules, playing a crucial role in cancer treatment.

Topoisomerase inhibitors can lead to cell death by preventing the relaxation of supercoiled DNA.

Chemotherapeutic agents aim to kill cancer cells more effectively than normal cells, ensuring minimal harm to healthy tissue.

Alkylating agents attach alkyl groups to DNA, causing cross-linking that damages DNA and leads to cell death.

Cyclophosphamide and ifosfamide are typical alkylating agents with various side effects, including myelosuppression and nausea.

Platinum compounds, such as cisplatin, work by cross-linking purine DNA bases and have side effects like nephrotoxicity.

Nitrosoureas, related to mustard gas, cause pulmonary toxicity and central nervous system problems.

Antimetabolites inhibit DNA replication by mimicking normal cell compounds and are specific to cells in the S phase.

Methotrexate, a folate inhibitor, is commonly used and requires leucovorin to protect healthy cells from its effects.

5-FU, a pyrimidine inhibitor, causes myelosuppression and GI problems depending on its administration method.

Capecitabine is an oral prodrug for 5-FU, and its side effect includes hand-foot syndrome.

Microtubular targeting agents, like vinca alkaloids, inhibit mitosis by destroying microtubules, preventing chromosome separation.

Taxanes stabilize microtubules, preventing their function and leading to cell death by disrupting chromosome separation.

Anthracyclines have a multifaceted mechanism of action, including intercalating DNA and generating reactive oxygen species.

Monoclonal antibodies are synthesized to target specific receptors known to inhibit cancer growth.

Rituximab targets CD20, commonly used to treat lymphomas, and is an example of a monoclonal antibody.

Bevacizumab targets VEGF and is used for solid tumors, with a side effect of GI perforation due to its mechanism of action.

Hormonal therapies, such as tamoxifen for breast cancer and anti-androgens for prostate cancer, target hormone production to inhibit cancer growth.

Transcripts

this is a short video on

chemotherapeutic agents we have a few

scattered pictures and diagrams here to

start on the left we have vinka alids

and taxanes which are two classes that

affect microtubules we'll talk about how

those affect macrotubes and and the

action of killing cancer we have in the

middle the two Topo isomerase Inhibitors

and we're going to talk about how those

can lead to cell death as long as well

as a couple examples of those and on the

right here we have a general graph that

shows how when we use chemotherapeutic

agents we want to ensure that they kill

cancer cells better than they kill

normal cells so we're going to jump

right into talking about the classes of

these chemical agents used in the

treatment of cancer this is

chemotherapeutic

Agents we're going to start with alkala

agents first this is the first class

we're going to be talking about now

alkala agents in general attach alkal

groups to DNA they usually attach groups

between two base pairs allowing for

cross-linking of base pairs this of

course damages the DNA makes you unable

to replicate it and it kills the cell

that way now the good thing about

ulating agents is that they they are not

specific to any part of the cell cycle

so they should be working on all cells

regardless of what part of the cell

cycle they're

in we have some common typical alkala

agents here we have typical and atypical

alkala agents we're going to start

talking about the typical ones the two

that are that are important to know are

cyclophosphamide and if phosphamide now

there's a whole list of side effects

with these and a lot of them are the

ones that you might classically think of

as side effects to chemotherapy we have

Milos supression which means a drop in

white blood cells a drop in hemoglobin

and a drop in the crits we have nausea

and vomiting that's the big one

Everybody's scared of nausea and

vomiting when getting chemo we have

secondary malignancies we have

infertility and hemorrhagic cystitis

which is a problem with the kidneys you

get blood in the urine and you have pain

with urination um it's caused by the

irritation of the bler from the acryline

metabolite now we have atypical alkala

agents as well we're going to start off

by talking about the Platinum compounds

these work by coal binding purine DNA

bases we're going to talk about three of

these first we have cisplatin which has

side effects of nephrotoxicity and

nausea and vomiting this is actually the

strongest inducer of nausea and vomiting

that we're going to be talking about

today it's extremely poent potent and it

it almost certainly causes vomiting in a

patient if you don't give them any

medication for for vomiting when you're

administering cisplatin we have carop

platin which causes platelet problems

and we have oxop platin which causes

cold sensitivity and it's worth

mentioning that all of these Platinum

compounds also cause peripheral

neuropathies or like a like the pins and

needles tingling in your in your fingers

and fingers and toes next group of

atypical alkala agents are the nitroso

uras now these are two acronyms bcnu

ccnu the actual names for these drugs

have mus in them M like car musine it's

because they are related to mustard gas

that was used during one of the world

wars so it's easy to remember that these

which are related to mustard gas if you

look up the full names of them cause

pulmonary toxicity and it's also worth

mentioning that they also cause fitis

and central nervous system problems so

these are the alkala agents next we're

going to talk about antimetabolites we

also have three categories of these but

first antimetabolites inhibit DNA

replication by mimicking normal cell

compounds and because these are

inhibiting DNA replication they are

specific to cells that are in the S

phase because you undergo DNA repli

replication in the S

phase first group we're going to talk

about is folate Inhibitors and the big

one here is methotraxate very commonly

used drug it inhibits dihydrofolate

reductase which is an enzyme that

prevents the Regeneration of

tetrahydrofolate and it inhibits the

conversion of folate which is a dietary

supplement something that we get from

our food into

tetrahydrofolate when when we administer

Methotrexate we always want to do it

with lucor lucor is an adant that

protects the healthy cells it actually

gives the healthy cells another method

of getting folate another method of

using folate and uh Methotrexate and

lucor go together for that reason side

effect of Methotrexate is mucositis and

Milo supression Milo suppression is

going to come up quite a bit next group

of antimetabolites are the peridian

Inhibitors big one here is 5fu five fluo

urasil which inhibits the enzyme

thymidilate

synthetase when you administer 5fu as a

Bolis it's going to cause Milo

suppression if you administer it in a

continual dose it's going to cause GI

problems like diarrhea mucositis so the

side effects of 5fu depend on how you

administer it you also want to use lcav

Orin with 5fu for a different reason

this time this time lcav Orin helps the

mechanism of action of 5fu when you use

methotraxate and lucor lucor protects

the healthy cells when you use 5fu and

Lorin lucor potentiates the mechanism of

action of 5fu it's worth noting the

difference of lucor between its use in

Methotrexate and five floro

uracil Cape cabine is essentially an

oral prodrug for 5fu now 5fu normally is

not administered orally cap cadine is a

pro drug which means that it must be

further processed in the body before it

becomes active and that's cap citadine

one of the side effects of cap citadine

is hand foot syndrome your palms and

your feet become red they can start

blistering and the last of the

perimidine Inhibitors is

cabine which is a rabinos c it's a DNA

chain

Terminator side effect here is

conjunctivitis and cerebral neural

defects so a or cabine causes

conjunctivitis and cerebral defects so

CCC a conjuntivitis cerebral neural

defects it's also worth mentioning that

cabine is the seven and seven plus

chemotherapy if you haven't heard of

that it's like a 10-day regimen of

chemotherapy that's very common for the

first seven days you're going to be

administering cabine and that's before

three days of anthracyclin we'll talk

about anthracyclin in a

second and there's one other class of

antimetabolites called the purine analog

and the one that is important to know is

six mapto purine easy to remember that

as a purine analog six

mercaptopurine so we have three classes

of antimetabolites which is a larger

class of therapeutic drugs we have

folate Inhibitors perimidine Inhibitors

and purine

analoges now another class microtubular

targeting

agents these drugs inhibit mitosis

mitosis of course uh occurs during the

mphase they uh specifically Target the

microtubular activity during mitosis

we're going to talk about how they do

that vinka alids firstly destroy

microtubules easy to remember vinka

alids destroy microtubules and that

obviously prevents their function three

vinka alids are listed here blast is

underlined you'll see why in a second

side effects of vinka alids are

peripheral neuropathy and Milo

suppression blast is the strongest of

the of those three in suppressing the uh

the the immune system so BL Vin VIN

blastin is the strongest Milos

supressive chemotherapeutic drug it has

the strongest side

effect one important thing to remember

about vinka alids is that you cannot

inject them directly into the spine they

are fatal if given intrathecally

next group of microt tual targeting

agents are the tanses these stabilized

microtubules which prevent them from

doing what they actually need to do

which prevent the microtubules from

actually touching the chromosomes and

pulling them apart during metaphase so

vinka alids destroy them tanes stabilize

them both render them

useless two Texans that are important to

know were pexel and dosex side effect of

these are mild suppression we're going

to be seeing that a lot and peripheral

neuropathies there's also hyper

sensitivity associated with these and

it's important to note that the hypers

sensitivity doesn't come from the drugs

doesn't come from pxel and doxal

directly but rather it comes from the

diluents that the drugs are dissolved in

these diluents cremophor and tween80

both cause hypers sensitivity the one

from pcxl cremor is a little more

potent if we don't want to deal with

this hypers sensitivity we could also

administer a braan which is a different

formulation of pxel it's protein bound

pxel and it helps us avoid hypers

sensitivity that's involved with the

cremor diluent in pet

axel one of the trade-offs of using

abraxane versus pet Axel is that you

have more neuropathy so you have less

hypers sensitivity but more

neuropathy next class toois Inhibitors

there's Topo isomerous one Topo isas 2

the ones that inhibit Topo one prevent

the relaxation of super coil DNA two of

these to remember Topo tan and irin

iroan iroan has a fun pneumonic to help

you remember what it does we'll get in

that in a second both of these cause myo

suppression like almost everything else

we're talking about iroan causes

diarrhea e it remember because ireno

Tean sounds like I ran to the can you

ran to the can when you have diarrhea

caused by

aroan Topo 2 inhibitors prevent

recoiling of DNA after transcription

couple of these to remember are toide

and teniposide both ending in ide Topo

isas two Inhibitors both have side

effects of M suppression mucositis and

secondary malignancies such as causing

AML acute acute myoblast leukemia these

are the three fourm that are associated

with topo2 Inhibitors such as etoposide

and teniposide

next class that we want to talk about

are the

anthracyclines anthracyclines kind of

have an ambiguous mechanism of action

they do a bunch of stuff they could do

more than one of these they could just

do a few of these some of them are

listed here they can intercalate DNA

which means that they insert themselves

between the actual the two actual

strands of DNA preventing their

replication and preventing synthesis of

RNA from that DNA so they intercalate

DNA and just inhibit the use of that DNA

they can also inhibit too isomerase 2

one of them do rubinson uh in particular

inhibits do or inhibits topoisomerase 2

they can generate reactive oxygen

species that cause oxidative damage to

the DNA and they also might cause alkal

which like we saw with the alkala agents

can cause cross-linking between DNA

based Pairs and uh and essentially

render the DNA useless kind of like

intercol of DNA anthocyans are easy to

remember because they all end in rubison

these are the rubinson dxor rubinson

Donar rubison you can read the rest

there Ida rubenson and EP rubison side

effects of these are pretty common to

all of them B ventricular heart failure

and this is based on the dose the

cumulative dose of the rubison

administered so there's like a limit for

each of these Rubin so Dr ubon's limit

might be some number you can only give a

person so much doxy rubenson before they

hit that number and be at a

statistically significant increase risk

for biventricular heart failure one

other side effect for the anthocyans is

that they are necrotic with extrav this

means that if you when you're normally

injecting these into the veins if you

miss the veins and accidentally get some

of these anthy into the surrounding

tissue they can cause necrosis of that

tissue leave very nasty looking wounds

they could tear up somebody's whole arm

tear up somebody's wrist if you miss

when inserting a vein so nurses are

trained really well to to be very

careful about administering anthres if

you want to look up some pictures of

this it looks pretty nasty it's kind of

fun to look at uh you can you can look

up anthy extravasion and it should be

pretty easy to

find it's also worth noting that

anthocyans are the three in the

aforementioned 7 plus three chemotherapy

so you have seven days of cabine

followed by three days of one of the

anthocyans such as duct

rubenson next class are the monoclonal

antibodies these are antibodies that are

synthesized to a specific Target that

has been known to inhibit cancer we'll

give you a bit more detail here the

origin of the monocolonal antibodies can

be determined from the suffixes so monal

antibodies ending in omab Come From Mice

or Mouse is easier to remember the O

from omab o from

Mouse the xab ending or imab uh comes

from the

chimeric antibodies these chimeric

antibodies are a cross between human and

mouse so they have some human in them

this list by the way is is in decreasing

order of how much mice is involved in

these antibodies so this umab this next

one is humanized which means it's about

10% Mouse 90% human easy to remember

because umab has a u in it just like

human then finally the fully human

antibodies are called mumab now these

mums are 100% human so I believe the the

chimeric antibodies are about 33% human

the humanized antibodies are about 10%

human and the fully human antibodies

excuse me the umab antibodies are about

10% Mouse and the fully human antibodies

are about 0%

Mouse we have a list of four important

monoclonal antibodies that are that are

probably worth knowing uh start with

rmab very commonly used it targets cd2

which is a receptor very common to B

cells it's used to treat lymphomas or

the abnormal proliferation of B cells

that you often see in lymphomas and

we're not going to we're not going to be

discussing the toxicity for the first

two but Target cd20 used for

lymphomas there's another one used for

breast cancer targets her too also not

as not as significant camab targets the

egfr receptor andth thelial growth

factor receptor this is uh used to treat

solid tumor and it was initially

developed to treat color rectal cancer

one of the side effects of camab is that

you get hypers sensitivity in the form

of an acneform rash so it looks like you

have dots all over your skin you get a

rash if you use camab another one that's

worth knowing is Bez

bevacizumab which targets VF which is a

vascular endothelial growth factor also

used for solid tumors um initially

developed for coloral and lung cancers

this is a problem because it can cause G

ey perforation VF is a factor that

promotes angiogenesis promotes the

growth of of blood vessels into new

parts of the body or into tumors if you

inhibit those you can weaken the GI

tract and cause perforation of the GI

tract and finally we're going to have a

short list of other chemotherapeutic

agents bomy is worth noting because it

causes lung toxicity just like the the

ones related to mustard gas that we

talked about earlier the nitroso uras

bomy also causes long

toxicity side effects of this long

toxicity include pulmonary fibrosis

interstial pneumonitis and hypers

sensitivity pneumonitis which includes

cough for having infiltrates in the

lungs and there are a couple other

hormonal therapies that are worth

knowing some of these are for breast

cancer specifically the

antiestrogens such as tamoxifen and the

aromatase inhibitor

rheumatism I don't think I have any

examples here but they block the

synthesis of estrogen actually there are

a couple examples ending in OZO so the

one that's important to know is the

anti-estrogen

tamoxifen there are also some hormonal

therapies for prostate cancer such as

the anti-androgens and there should be a

small list of these like the LH RH

antagonists or excuse me lhrh agonists

the GnRH antagonists and the cyp17

Inhibitors and if you look up the

production of testosterone you can kind

of see how these three subclasses of

anti-androgens all kind of inhibit

testosterone production in a different

way all with the evental goal of

preventing Androgen stimulation of

prostate cancer so these are other

chemotherapeutic agents that didn't

really fit into the other categories

this has been a brief review of

chemotherapy agents I hope it was

helpful and I hope it was uh good a good

introduction to to commonly use drugs

and their mechanisms of actions and side

effects thanks for listening