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126 Cards in this Set
- Front
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Carbamazepine
(uses, side effects) |
Na channel antagonist
Treats partial seizures (esp. complex), tonic-clonic Induces p450 (i.e. CYP3A4) SE: Leukopenia, diplopia, (hepatotox, coma) (Anti-epileptic, use dependent for better channel selectivity, decrease depolarizing current) |
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Lamotrigine
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Na channel antagonist
(Anti-epileptic, use dependent for better channel selectivity, decrease depolarizing current) |
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Oxcarbazepine
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Na channel antagonist
(Similar side effects as Carbamazepine: nausea, diplopia, drowsy, but less p450 induction and toxicity) (Anti-epileptic, use dependent for better channel selectivity, decrease depolarizing current) |
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Phenytoin
(use, side effects) |
Na channel antagonist
Widely used (partial, tonic-clonic-status, epilepticus, NOT absence) Highly bound to albumin; if another drug given could outcompete it=raise [free phenytoin] Induce p450 metabolism SE: Hirsutism, neuropathy, ataxia, gingival hyperplasia (Anti-epileptic, use dependent for better channel selectivity, decrease depolarizing current) |
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Topiramate
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Na channel antagonist
(Anti-epileptic, use dependent for better channel selectivity, decrease depolarizing current) |
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Valproate
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Na channel antagonist, Ca (T-type) channel antagonist, GABA-A agonist
Good for kids SE: weight gain, tremor, polycystic ovaries, anovulatory cycles, encephalopathy |
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Zonisamide
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Na channel antagonist
(Anti-epileptic, use dependent for better channel selectivity, decrease depolarizing current) |
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Ethosuximide
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Ca channel antagonist used to treat ABSENCE (epilepsy)
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Mechanisms of action for anti-epileptics (4)
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Block initiation or spread of abnormal electrical discharge
1) Block Na channels 2) Block Ca channels 3) Enhance GABAergic impulses 4) Interfere w/glutamate transmission |
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Primary v. Secondary epilepsy
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Primary: no anatomic cause; ideopathic; treated chronically w/drugs
Secondary: tumors, head injury, infection, etc. (often reversible) |
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Partial (Simple vs. Complex) seizures
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Partial: symptoms depend on site of neuronal discharge (can spread and become generalized tonic clonic)
Simple partial: does not spread; conscious; localized abnormal muscle movements; sensory distortions Complex partial: consciousness altered, motor dysfunction, incontinence |
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Generalized seizure
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Begin locally and rapidly spread to both hemispheres (convulsive or not; usually lose consciousness)
(Types: 1. tonic-clonic 2. absence 3. myoclonic 4. febrile seizures 5. status epilepticus) |
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Tonic-clonic/grand mal (generalized)
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Tonic (stiff) followed by clonic (rapid contraction/relaxation); lose consciousness
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Absence/petit mal (generalized)
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Self-limiting, brief loss of consciousness; staring spells; often onset 3-5 yo til puberty.
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Myoclonic seizure
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Short episodes of muscle contractions (rare, often result of neurological damage)
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Status epilecticus
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Life-threatening condition; seizures are rapidly recurrent
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Phenobarbitol
(uses & side effects) |
GABA-A receptor agonist (barbiturate)
Uses: NOT absence seizures (alternative for simple partial, tonic-clonic, status epilepticus) Induce p450 SE: Sedation, cognitive decline (↑ duration of GABAA R opening so let in more Cl-) |
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Valproate
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Na antagonist, Ca (T-type) channel antagonist, GABA-A receptor agonist
(Best for myoclonic seizures; 2nd choice for absence) |
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Topiramate
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GABAA receptor agonist
(GABA + GABAA Receptor → open channel → Cl- influx →hyperpolarization) |
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Felbamate
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GABAA receptor agonist
(GABA + GABAA Receptor → open channel → Cl- influx →hyperpolarization) |
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Benzodiazepines
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↑ frequency of GABAA R opening
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Mechanism of antidepressants
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Potentiate actions of norepinephrine and/or seratonin in the brain
(While these drugs can increase levels of NE/seratonin almost immediately, effects take weeks. Proposed that presynaptic inhibitory receptors densities decrease after weeks of antidepressant use. Permits greater synthesis/release of NTs. |
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Depression (what is believed to cause it)
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Deficiency of monoamines (NE and seratonin) at certain sites of the brain that control mood/emotions
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Reserpine
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Was used to treat HT (it depletes monoamines like NE and seratonin in the synapses peripherally and in CNS)
SE: severe depression bc of effects in CNS (offers support to theory that depression is due to NE/seraonin deficiency in brain) |
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MAOI Antidepressants (mechanism and side effects)
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Inhibits monoamine oxidase (MAO) so less monoamine degredation (more NE/seratonin in cleft)
SE: Orthostatic hypotension insomnia TYRAMINE: MAO needed to break down ingested tyramine→tyramine in enters neuron terminal via Uptake1→displaces/pushes out catacholamines into synapse→Hypertensive crises: tachycardia, headache, stiff neck, arrhythmia, seizure, stroke |
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Isocarboxazid
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MAOI (treat depression, esp. atypical)
SE: Orthostatic hypotension, HT crisis with tyramine |
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Phenelzine
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MAOI (treat depression, esp. atypical)
SE: Orthostatic hypotension, HT crisis with tyramine |
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Tranylcypromine
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MAOI (treat depression, esp. atypical)
SE: Orthostatic hypotension, HT crisis with tyramine |
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Selegiline
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MAOI (treat depression, esp. atypical)
Transdermal (bypass GI so avoids tyramine diet restriciton) |
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Tricyclic Antidepressants (mechanism, uses, side effects)
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Mech: inhibits reuptake of NE and serotonin into presynaptic nerve terminals
Use: usually for depression when SSRIs fail. Also for: Anxiety Disorders Bulimia Nervosa Migraine / tension headaches Pain Disorders Irritable Bowel / visceral hypersensitivity. Pruritis (doxepin) Urticaria (hives) SE: Muscarinic blockade: (Blurred vision, dry mouth, urinary retention, constipation, narrow angle glaucoma Block alpha-adrenergic receptors: orthostatic hypotension, dizziness, tachycardia Cardiac arrhythmias (ecgs over 45) Small therapeutic index (don’t dispense large amounts of TCAs bc can be used for suicide) |
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Imipramine
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Tricyclic antidepressant
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Doxepin
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Tricyclic antidepressant
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Amitriptyline
Nortriptyline Doxepin Clomipramine Imipramine Desipramine |
Tricyclic antidepressants
Desipramine is metabolized by CYP2D6 |
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SSRI (mechanism, uses, side effects)
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Mech: block reuptake of serotonin
Depression Panic Disorder Generalized Anxiety Disorder Obsessive Compulsive Disorder Social Phobia PTSD Bulimia Nervosa SE: GI (Nausea, vomiting, diarrhea) Sexual Dysfunction “Anxiety” Sleep Disturbance Headaches (Possibly increased sucidal ideation/seratonin toxicity) |
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Serotonin toxicity
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Mental confusion, hallucinations, headache, coma, shivering, sweating, hyperthermia, hypertension, tachycardia, nausea, diarrhea, hyperreflexia, tremor.
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Citalopram
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SSRI Antidepressant
SE: GI (Nausea, vomiting, diarrhea) Sexual Dysfunction “Anxiety” Sleep Disturbance Headaches (Possibly increased sucidal ideation/seratonin toxicity) |
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Escitalopram
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SSRI Antidepressant
SE: GI (Nausea, vomiting, diarrhea) Sexual Dysfunction “Anxiety” Sleep Disturbance Headaches (Possibly increased sucidal ideation/seratonin toxicity) |
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Fluoxetine
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SSRI Antidepressant
Inhibit P450 enzymes, especially 2D6 (metabolized by 2D6) (Activating=insomnia) SE: GI (Nausea, vomiting, diarrhea) Sexual Dysfunction “Anxiety” Sleep Disturbance Headaches (Possibly increased sucidal ideation/seratonin toxicity) |
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Fluvoxamine
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SSRI Antidepressant
SE: GI (Nausea, vomiting, diarrhea) Sexual Dysfunction “Anxiety” Sleep Disturbance (Sedative) Headaches (Possibly increased sucidal ideation/seratonin toxicity) |
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Paroxetine
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SSRI Antidepressant
Inhibit P450 enzymes, especially 2D6 (metabolized by 2D6) SE: GI (Nausea, vomiting, diarrhea) Sexual Dysfunction “Anxiety” Sleep Disturbance (sedative) Headaches (Possibly increased sucidal ideation/seratonin toxicity) |
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Sertraline
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SSRI Antidepressant
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SNRIs (mechanism, side effects)
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Serotonin/Norepinephrine re-uptake inhibitors
SE: Nausea Insomnia Headaches High blood pressure Sexual dysfunction |
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Duloxetine
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SNRI
Use: (Depression) (Generalized Anxiety) Diabetic neuropathy Fibromyalgia |
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Venlaflaxine
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SNRI
Use: (Depression) (Generalized Anxiety) Panic Disorder Social Phobia |
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Bupropion
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Atypical antidepressant
Uses: Depression Smoking cessation Not as useful for anxiety SE: Seizure risk Pros: less sexual disfunction, no weight gain |
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Mirtazapine
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Atypical antidepressant
Blocks pre-synaptic alpha-2 receptor Antihistamine properties lead to: sedation, weight gain |
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Nefazodone
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Atypical antidepressant
No weight gain, hepatotox (not used much) |
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Trazodone
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Atypical antidepressant
Strong sedative (use at night for insomnia with SSRIs) Priapism |
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Main side effect: MAOIs
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Tyramine ingestion=stroke/death
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Main side effect: Tricyclic antidepressants
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Overdose=cardiac arrest
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Main side effects: SSRIs
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nausea, diarrhea, insomnia, sexual problems
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Main side effect: SNRIs
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nausea*, headache, sexual problems*
*same as SSRI |
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Main side effect: Bupropion
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Too much=seizure
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Main side effect: Mirtazapine
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Sedated, weight gain
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Main side effect: Trazodone
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Priapism
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Main side effect: Nefazodone
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Hepatotox
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Carbamazepine
Lamotrigine Oxcarbazepine Phenytoin Topiramate Valproate Zonisamide |
Na channel blockers (anti-epileptic)
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Valproate
Ethosuximide Gabapentine |
Ca channel blockers (anti-epileptic)
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Benzodiazepines
Topiramate Valproate Felbamate Phenobarbital (barbituate) |
GABA receptor agonists (anti-epileptic)
Benzodiazepines → ↑ frequency of GABAA R opening Barbiturates → ↑ duration of GABAA R opening (ex. Phenobarbital) |
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Clomipramine
Amitriptyline Nortriptyline Doxepin Imipramine Desipramine |
Tricyclics
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Selegiline
Phenelzine Isocarboxazid Tranylcypromine |
MAOIs
Selegiline is transdermal |
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Sertraline
Citalopram Fluoxetine Fluvoxamine Escitalopram Paroxetine |
SSRIs
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Duloxetine
Venlafaxine Desmethylvenlafaxine |
SNRIs
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Bupropion
Mirtazapine Nefazodone Trazodone |
Atypical Antidepressants
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Main antidepressants (4) metabolized by CYP2D6
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Fluoxetine (SSRI)
Paroxetine (SSRI) Desipramine (Tricyclic) Nortriptyline (Tricyclic) |
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If inhaled anesthetic is very lipid soluble, it will...
1) be more/less potent? 2) have high/low MAC? 3) have fast/slow onset? 4) effective at high/low partial pressure in CNS? |
Lipid soluable...
1) MORE potent 2) LOW MAC 3) SLOW onset 4) effective at LOW partial pressure |
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Malignant hyperthermia (cause and treatment)
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Cause: Rare abnormality of ryanodine receptor in SR. Volatile anesthetics can cause hypermetabolic response of skeletal muscle.
Symptoms: pyrexia, increased CO2 production, rigidity, cardiovascular collapse, death. Treatment: Dantrolene |
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4 components of anesthesia
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analgesia - absence of pain
amnesia - absence of memory hypnosis - absence of awareness immobility - absence of movement |
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Rate of anesthetic elimination from body depends on these 2 factors
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Solubility (soluble=slow elim)
Duration of anesthesia (long duration=slow elim) |
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Ether
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Inhaled anesthetic
Pros: Spontaneous breathing/open airway Muscle relaxation Circulatory stability, safe Cons: Explosive Vomiting Slow, unpleasant induction |
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Nitrous oxide
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Inhaled anesthetic
Pros: Rapid onset/offset Very little toxicity Cons: Low potency (needs to be used w/other anesthetics) |
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MAC
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Minimum alveolar concentration
PARTIAL PRESSURE at which 50% of patients don't move (Low MAC=more potent) |
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Propofol
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IV Anesthetic
Pro: Rapid metabolism (quick offset, used as continuous infusion) Cons: Respiratory/cardiac depression Pain w/IV injection Expensive Other: Lipid soluble |
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Ketamine
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IV Anesthetic
Pros: Spontaneous breathing (good for kids/unstable patients) IM injection (water soluble; use for uncooperative patient) Cons: Psychic effects Other: Bronchodilator Stimulate sympathetic NS (increase BP/HR) |
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Thiopentol
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IV Anesthetic
Pros: Proven record Cheap Cons: Prolonged effect w/repeated use Respiratory/cardiac depression (Triggers prophyria) |
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Do very lipophilic IV anesthetics have a FAST or SLOW onset/offset in the brain?
Are they cleared out of the body QUICKLY or SLOWLY? |
Fast onset in the brain (opposite of lipophilic inhaled anesthetic)
Cleared slowly as stored in fat and muscles after anesthetic levels drop in brain. (These properties have nothing to do with metabolism, just lipophilic) |
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Inhaled anesthetics: clinical uses
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1) Induction anesthesia (children/fear of needles)
2) Maintenance anesthesia |
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Inhaled anesthetics: side effects
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Respiratory depression (decrease pump function)
Upper airway muscles relax (obstruction) Bronchodilator Decrease BP (vasodilate, depress baroreceptors, depress myocardial contractility) Some effects beneficial if have MI as they decrease O2 demand of heart Halothane Hepatitis: rare; immune response results in fulminant hepatic necrosis Malignant hyperthermia |
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Inhaled anesthetics (5)
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Isoflurane
Halothane (most potent/lowest MAC) Desflurane Sevoflurane Nitrous Oxide (least potent/highest MAC) |
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Eicosanoids
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Arachadonic acid derived autocoids; inflammatory mediators
Prostaglandins (COX-1&2), leukotrienes (5-lipoxygenase) All are lipid derived (phospholipase A2 on plasma membrane phospholipids) (autocoid=biologically active substance with a short half-life that acts near site of synthesis) |
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COX-1 effects
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At physiologic levels eicosanoids regulate:
platelet aggregation maintenance of the gastric mucosa vascular homeostasis kidney function DETAILS: Vasodilation (PGI2, PGE2) Decrease gastric acid (PGI2) Increase gastric mucous (PGE2) Decrease platelet aggregation (PGI2) Increase platelet agg (TXA2) Vasoconstriction (TXA2) (Constitutively expressed in GI mucosa, vasculature, platelets) |
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COX-2 effects
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Increase pain sensation (PGE2)
Fever (PGE2) (Expression induced by inflammatory stimuli in pro-inflam cells; responsible for undesired increase in prostaglandins during inflam) |
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NSAIDS (5)
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Nonsteroidal Anti-Inflammatory Drugs:
Salicylates (Aspirin) Ibuprofen (Advil and Motrin) Naproxen (Aleve) Acetaminophen (Tylenol) COX-2 inhibitors (Vioxx and Celebrex) (Non-selectively block COX-1&2; most adverse effects due to inhibition of COX-1) |
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5-Lipoxygenase main effect
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Bronchoconstriction (Leukotrienes)
Can cause asthma! |
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What general class of molecules cause increased pain sensation, fever, and inflammation?
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Excess prostanoids
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NSAIDS (desired/undesired effects)
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Desired (due mostly to COX-2 inhibition):
Anti-inflammatory (decrease vasc tone) Analgesic Antipyretic Undesired (due mostly to COX-1 inhibition): Decreased gastric mucous production Decreased platelet aggregation (prolonged bleeding time) Increased vasc tone (acute renal insufficiency/nephritis if chronic high dose) Rash Hepatotox (overdose acetomeniphen) Increase risk MI/stroke with COX-2 selective inhibition (Vioxx/Celebrex) |
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What NSAID irreversibly inhibits COX-1&2?
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Aspirin (Salicylate)
(much more selective for COX-1 so more side effects than NSAIDS like naproxen) |
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Aspirin adverse effects
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Reyes Syndrome:
Aspirin given to child/adolescent with viral fever. Vomiting, confusion then stupor, fatty liver then coma/death. No cure, 50% die. Upper GI bleed: Directly damage (weak acid) Indirectly damage from inhibiting COX-1 (increase acid, decrease mucous) |
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COX-2 selective NSAIDS (pros/cons)
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Pro:
Reduce the unwanted effects of COX-1 inhibition, w/o losing the desired anti-inflammatory effects of COX-2 inhibition Cons: increase risk of adverse thrombotic cardiovascular events (stroke, MI) |
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Misoprostal
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Synthetic Prostanoid
Use: -Prevent NSAID induced peptic ulcers (enhance PGE=increase mucous, decrease acid) -Maintain PATENT DUCTUS ARTERIOSUS if have transposition of great vessels -Labor induction Adverse effects: Abortifacient (don't give to pregnant woman) Diarrhea |
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Acetaminophen
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NSAID (tylenol)
Use: fever in younger than 16 (not aspirin), pain, NOT an anti-inflammatory (only active in CNS where enzyme is present, not periphery) Hepatotox in high doses |
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Indomethacin
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Potent NSAID
Close Patent Ductus Arteriosus |
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Zileuton (Zyflo)
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Leukotriene Antagonist
Prophylactic treatment of asthma (inhibit 5-lipoxygenase, decreasing leukotriene synthesis so LESS bronchoconstriction) Some hepatotox |
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Montelukast (Singulair) and Zafirlukast (Accolate)
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Leukotriene Antagonist
Prophylactic treatment of asthma Seasonal allergies (block leukotriene binding) SE: Some hepatotox *Churg-Strauss syndrome (autoimmune vasculitis)* |
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Types of genotoxic stress (5)
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1) Base modification
2) DNA crosslinks (intra/interstrand) 3) Protein crosslinks 4) Single/double strand breaks 5) Replication stress (stall DNA polymerase; can result in single strand) |
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DNA damage can arrest cell cycle in...
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G1, S, G2 to M
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Pathway for DSB repair? Path for excessive ssDNA?
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DSB-->ATM (DNA repair) phosphrylates/stabilizes p53 (arrest in G1, death if can't repair)
ssDNA-->ATR (DNA repair) activates Chk1 (DNA repair, S-phase arrest, G2 arrest) *DNA repair/processing can convert DSBs to ssDNA and vice versa* |
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What causes double strand breaks (DSB)?
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1) Normal DNA metabolism (i.e. meiotic recombo)
2) Ionizing radiation (ssDNA breaks but close together so effectively is DSB; electrons reacts with H2O to make clouds of OH radicals) |
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What's ATM?
What activates it? What's it do? What if it's mutated? Arrest in which part of cycle? |
ATM is a protein kinase tumor suppressor
Activated by DSB in DNA Leads to DNA repair, cell cycle arret in G1 (checkpoint), and can cause cell death if can't repair) Phosphorylates and stabilizes *p53* (p53 leads to G1 arrest and/or cell death) If mutated, sensitive to DSB (not other stuff like UV). People with Atxia-Telangiectasia have mutated ATM. G1 arrest |
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p53
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p53 is a transcription factor that transcription factor that binds DNA and induces the transcription of specific genes that regulate DNA repair, apoptosis, cell cycle arrest, etc.
Stabilized/phosphorylated by ATM Activate p21 which... -Inhibits Cdk4/5 and cyclin D -Inhibits Cdk2 and cyclin E *This makes cell stuck in G1 |
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What results in ssDNA?
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Anything that inhibits replication
*Block DNA polymerase (helicase keeps unwinding ahead) -DNA break -Crosslinked DNA (cisplatin) -Block dNTP production -Gemcitabine (incorporated into DNA) |
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What's ATR?
What activates it? What's it do? Arrest in which part of cycle? |
ATR is a protein kinase tumor supressor
Activated by ssDNA Phosphorylates and activates Chk1 (kinase). Chk1 activates stuff to block... *Cdk2/cyclin A=arrest in S phase *Cdk1/cyclin B=arrest in G2 |
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Radiotherapy
(how used and what can make cells resist it) |
Give many small doses (normal cells can recover faster than tumor cells)
ATM can help tumor cells recover from the double strand breaks (ATM inhibitors could enhance tumor response) |
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Cisplatin
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Chemotherapeutic rug that creates intrastrand crosslinks. Stall DNA polymerase to create ssDNA. ssDNA activates ATR-Chk1 (arrest in S or G2).
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Block dNTP production as cancer treatment
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Stops DNA polymerase bc run out of dNTPs for new DNA. Results in ssDNA (activate ATR-Chk1 to stop in S or G2)
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Gemcitabine
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Gemcitabine is converted to gemcitabine triphosphate (Gem-TP) which is incorporated to DNA (looks like dCTP.
Stops DNA polymerase (activate ATR-Chk1) (Chk 1 inhibition increases sensitivity of tumor cells to Gemcitabine so more will die instead of successfully repairing) *Chk1 can help tumors survive genotoxic chemotherapy |
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Imatinib/Gleevec
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Inhibits bcr-abl
Treats chronic myelogenous leukemia (CML) (Use to treat CML with IFN + Cytarabine but gives flu like symptoms) |
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Bcr-abl
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Abl from chr9 goes to chr22
Bcr-abl kinase activates (hydrolyzes ATP to phosphorylate) multiple survival and proliferation pathways (Ras/Raf, Stat, Myc, Akt) |
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Imatinib/Gleevec resistance
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1) Bcr-abl copy number increases and is selected for
2) Bcr-abl active site for binding ATP or Gleevec mutated so Gleevec can't bind Other: Elevated P-glycoprotein (Mdr1) Elevated expression of kinases that can phosphorylate the activation loop of Bcr/abl Resistance can occur at several levels: -Altered drug uptake -Enhanced drug metabolism -Mutations that render the target less sensitive -Modifications in other pathways that bypass the inhibitor… *Can increase imatinib dose but eventually will need to get new drug |
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Nilotinib
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Bcr/abl kinase inhibitor with increased activity against Bcr/abl mutants
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Adjuvant therapy
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Eradication of tumor cells left behind after surgery (i.e. radiation)
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6 phenotypes associated with carcinogenesis
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1) Induce angiogenesis
2) Maintain telomeres during replication 3) Metastasize 4) Evade normal death signals 5) Disable normal cytostatic signaling mechanisms 6) Autonomously proliferate |
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Receptor tyrosine kinase (RTK) signaling pathways (general)
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Regulate differentiation, growth, proliferation, survival, metabolism, and cell movement
Richly populated with oncogenes and tumor suppressors Important driver of tumorigenesis |
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Outline RTK signaling pathway for Ras
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1) Initiate with receptor dimerization
2) Kinase activity of receptor phosphorylates other proteins 3) RTK phosphorylation at tyrosine creates docking site for SH2 4) SH2 binds Grb2/SOS complex 5) Grb2/SOS converts Ras-GDP to Ras GTP (GAP turns Ras off (GDP bound) 6) Ras activates MEK, activates ERK 7)ERK phosphorylates substrates that promote proliferation and survival (this path and other RTK paths result in: entry into cell cycle, growth, survival) RTK also turns on... -STAT activated -AKT activated |
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GAP
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Tumor suppresor that converts Ras-GTP to inactive Ras-GDP
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Ras is an oncogene when...
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...it's mutated to only bind GTP (always on)
(mutated in about 50% of tumors) |
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B-Raf is an oncogene when
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...mutated to be constitutively active (mutated in 60% of malignant tumors)
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PI3-K, PTEN, AKT
(which is oncogene, which is tumor suppressor?) |
PI3-K=oncogene (over expressed/active in tumors)
PTEN=tumor suppressor (turns off PI3-K and is inactivated in tumors) AKT=oncogene (turned on by PI3 and increases proliferation) |
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Outline PI3-K/AKT pathway
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1) PI3-K is activated by binding to phosphorylated RTK or GTP-Ras
2) PI3-K produces PIP3, a lipid second messenger 3) PIP3 activates the protein kinase AKT 4) AKT phosphorylates protein substrates that enhance survival 5) One AKT activates mTOR, which regulates the translation of mRNAs required for proliferation |
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Outline STAT pathway
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1) STAT binds phosphrylated tyrosine of RTK
2) STAT dimerizes and goes to nucleus to activate transcription |
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RTK signaling allows cell to enter which phase
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S (drive them past the restriction point in G1)
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cyclin D
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activates Cdk4 (RTK signaling induces cyclin D to enter S phase)
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ERK, STAT, AKT all promote...
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Cell survival (downstream in RTK signaling)
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Trastuzumab (Breast)
Cetuximab (Head and Neck, Colorectal) Bevacizumab (Colorectal, NSCLC) Panitumumab (Colorectal) |
Inhibit the RTK extracellularly (antibodies bind and inactivate the receptor to prevent proliferation)
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Gefitinib (NSCLC)
Erlotinib (NSCLC,Pancreatic) Gleevec (GIST, CML) Sunitinib (GIST, Renal) Dasatinib (CML) Lapatinib (Breast) |
Inhibit RTK intracellularly
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Rapamycin
Sorafenib |
Inhibit downstream in RTK signalling
Rapamycin inhibits parts of PI3-K path and MEK in Ras path Sorafenib inhibits Ras |
