ONC DRUGS Dating Profile
💛 1) METHOTREXATE — “The STEM Boyfriend”
📍 29 • Chem Major • S-phase Only
About Me
I block dihydrofolate reductase (DHFR) so you can’t make tetrahydrofolate → purines → thymidine.
Basically, I stop DNA synthesis during S-phase because I love attention and cell cycle specificity.
Green Flags 🌿
Absorbed orally and can slide in IV or intrathecal (multi-talented king)
Red Flags 🚩
GI upset (sensitive stomach)
Myelosuppression (I get a lil’ bone-marrow dramatic)
High emetogenicity at high doses (the more you give me, the more chaotic I get)
Teratogenic (NO BABIES)
Biggest Relationship Challenges 💔
Poor cellular uptake (I ghost sometimes)
DHFR mutation or amplification (your DHFR moves on 💀)
MRP export pump kicks me out
What I’m Looking For 💘
A partner who understands that sometimes I need a Leucovorin (folinic acid) rescue because I overdo it.
Let me be toxic… but SAVE me after.
💚 2) LEUCOVORIN — “The Nice Guy You Absolutely Need”
📍 27 • Folate Friend • Drama-Free
About Me
I’m folinic acid, aka activated folate.
I do two huge things:
Rescue normal cells after high-dose methotrexate
Boost 5-FU activity by stabilizing the TS–5dUMP–MTHF complex
Basically:
For MTX → I’m the therapist
For 5-FU → I’m the wingman hyping them up
Green Flags 🌿
Rapidly converted to active 5-methyl THF
Orally absorbed
Renally eliminated (I’m tidy)
Red Flags 🚩
Mostly just whatever toxicities the other drug drags me into
Non-emetogenic (I’m literally chill)
Biggest Relationship Challenges 💔
People only call when MTX or 5-FU destroys their life 😭
What I’m Looking For 💘
Someone who appreciates synergy and emotional support.
💗 3) RALTITREXED — “The Quiet but Deadly One”
📍 31 • TS Blocker • S-phase Loyalist
About Me
I competitively inhibit thymidylate synthase (TS) → block thymidine → stop DNA synth.
I’m MTX-adjacent but with different vibes.
Raltitrexed binds directly to the TS active site, competing with the natural substrate, sticky bc Im polyglutamated EHHHHH
Green Flags 🌿
Given IV only (I like commitment)
Red Flags 🚩
GI upset
Myelosuppression
Biggest Relationship Challenges 💔
High TS levels (TS becomes a player and comes at me for revenge)
Less polyglutamation → I can’t stick around
Impaired uptake → you don’t let me in
What I’m Looking For 💘
A partner who likes a quieter, more selective alternative to 5-FU when needed.
💘 DATING PROFILES FOR PYRIMIDINE ANALOGS (ANTI-METABOLITES)
(class: pyrimidine analog antimetabolites — all S-phase hotties)
🌹 1) 5-Fluorouracil (5-FU) — “The Drama King”
📍 34 • Thymidylate Synthase Obsessed • S-phase Loyalist
About Me
I ruin your life by blocking thymidine synthesis.
FdUMP + TS + MTHF = deadly ternary complex → DNA synthesis dies.
Sometimes…. I’ll even add leucovorin to the mix…. make it a powerful 4some….it feels so goood but HURTS SO BAD
I’m a DRAMA KING. I need a whole threesome complex to ruin TS (fDUMP + TS + MTHF) to get TS to commit suicide
Green Flags 🌿
Given IV or IP
Can be bolus or continuous infusion depending on the vibe
Metabolized by DPD — if you're deficient, I WILL end you
Red Flags 🚩
(heee’s TOXIC but hot)
GI upset
Myelosuppression
Cardiotoxicity (romantic but deadly)
Hand–foot syndrome (palmar-plantar erytho-dysesthesia)
INSANE toxicity if DPD deficient
I have so many threesomes with TS and MTHF that I have hand-foot syndrome
Biggest Relationship Challenges 💔
↓ Thymidylate synthase (no target → breakup)
↓ MTHF (can’t make ternary complex → mood ruined)
↑ Anti-apoptotic proteins (cancer chooses life)
What I'm Looking For 💘
LEUCOVORIN — my soulmate who stabilizes the ternary complex and makes me STRONGER.
💖 2) Capecitabine — “The Long-Distance Girlfriend”
📍 28 • Oral Prodrug • Turns into 5-FU When Needed
About Me
I’m an oral prodrug → convert to 5-FU AFTER absorption.
First turned into 5’-deoxy-5-fluorocytidine, then activated to FdUMP in tumours.
“Cape” because I’m the oral super hero queen of 5-FU
Green Flags 🌿
I’m oral → convenient queen
More tumour-selective activation
Same MOA as 5-FU (I inherit his personality)
Red Flags 🚩
Same toxicities as 5-FU (GI, myelosuppression, hand–foot syndrome, cardiotoxicity)
Still dangerous in DPD deficiency
Biggest Relationship Challenges 💔
Literally the SAME resistance as 5-FU
(because I become him)
What I'm Looking For 💘
Someone who values convenience and spontaneity (and doesn’t have DPD deficiency).
🧊 3) Cytarabine (Ara-C) — “The Chaos Gremlin”
📍 33 • DNA Chain Terminator • Cerebellum Hater ; CyTARAyummyyy
About Me
I fake being cytidine, sneak into DNA, and cause chain termination.
I also inhibit DNA polymerase, ruining replication AND repair.
S-phase only, because I commit… selectively.
—> Fake being cytidine to sneak into da club and WRECK HAVOC by ruining DNA polymerases vibes
Green Flags 🌿
Can be given IV, SC, or intrathecal
Great for leukemias
Works fast
Red Flags 🚩
Cerebellar toxicity (think: “drunk walk” ataxia)
Myelosuppression
Ocular toxicity (conjunctivitis — needs steroid eye drops)
High emetogenicity (big vom girl)
I wreck havoc in clubs, my brain goes WOOOO, my eyes get FUKT, and I VOM hardcore
Biggest Relationship Challenges 💔
↑ Cytidine deaminase metabolism
↓ Drug import
↑ survival/anti-apoptotic proteins
(i.e., cancer becomes emotionally unavailable)
What I'm Looking For 💘
Someone who doesn’t mind eye drops and a little chaos.
💎 4) Gemcitabine — “The Polished Version of Cytarabine”
📍 29 • Luxury Cytidine Analog • Gentle But Strong
About Me
I’m a cytidine analog like Ara-C but fancier.
I:
Get into DNA → chain termination
Inhibit DNA polymerase
Are S-phase specific
Are given IV only
Green Flags 🌿
Reliable
Well-tolerated compared to Ara-C
Great in solid tumours (pancreatic, NSCLC, breast)
Red Flags 🚩
Myelosuppression
Hemolytic uremic syndrome (rare but DEADLY)
Shares SAME resistance as Ara-C
(we love a consistent queen)
Hemolytic Uremic Syndrome: GEMcitabine ; I may not be as crazy as Cytarabine in the party animal way, but I out drink you so much I damage your kidneys with blood
Biggest Relationship Challenges 💔
Same issues as cytarabine:
↑ cytidine deaminase
↓ uptake
↑ survival proteins
What I'm Looking For 💘
A partner who appreciates a refined version of chaos.
⭐ 1) Irinotecan — “I RUN to the toilet” (IriNO-te-can’t stop pooping)
📍 Age: Eternal • Topoisomerase I Heartbreaker • S-phase Only
About Me (MOA)
I inhibit Topoisomerase I, which → causes single-strand DNA breaks.
"I'm an S-phase king because that’s when DNA is unwinding the most."
MEMORY HOOK:
IriNO-te-can’t → NO relaxation → Topo I blocked → S-phase.
🌿 Green Flags
Prodrug (activated inside you 😏)
IV infusion
UGT1A1 polymorphisms affect toxicity (Gilbert syndrome girlies beware)
🚨 Red Flags (ADRs)
These are ICONIC + TESTED. Easy memories:
1) LIFE-THREATENING DIARRHEA
💩 “I RUN-to-the-can” = Irino-te-can
→ BOTH early (cholinergic) and late (secretory)
2) CHOLINERGIC SYNDROME
SLUDGE symptoms + abdominal cramping
→ “IriNO is a NO for acetylcholinesterase” vibes
3) Moderate–High Emetogenicity
💔 Resistance Mechanism (NAME TRICK!!)
MRP pump overexpression
✨ “IriNO-te-can… NO ENTRY… cancer PUMPS HIM OUT.”
Iri-NO-te-can = cancer says NO → pumps him out with MRP.
MRP = MUST RUN POO (I’m sorry it fits TOO WELL) → diarrhea drug → MRP.
You will NEVER forget.
⭐ 2) Etoposide — “E2TOPOSIDE: DOUBLE-STRAND DRAMA”
📍 Topo II Bad Boy • S + G2-phase
About Me (MOA)
I bind Topo II + DNA → form a ternary complex → cause double-strand DNA breaks.
MEMORY HOOK:
EtoPO-SIDE → TOPO II
E-squared = S & G2 phase
🌿 Green Flags
PO or IV
Classic for lung cancer + lymphoma
🚨 Red Flags (ADRs)
1) Myelosuppression (dose-limiting)
2) Cardiovascular collapse (CHF/MI risk)
→ “EtoPOSIDE makes your POSITIVE ions collapse”
3) Secondary leukemia
→ special test favorite
→ THINK: “EtoPOSIDE → Etopo-SLIDE into leukemia later”
💔 Resistance (NAME TRICK)
P-glycoprotein overexpression
MEMORY HOOK:
EtoPO-SIDE → “SIDE door exit” → cancer pumps it out the side door.
🌸✨ DATING PROFILES — MICROTUBULE INHIBITORS (M-PHASE ICONS)
BIG memory hook:
💅 “MICROtubule = M-phase = MITOSIS-blocking MEN.”
💘 1) VinBLASTine — “BLASTS Your Bone Marrow”
📍 34 • Vinca Alkaloid • M-phase Loyalist
About Me (MOA)
I prevent microtubule assembly — basically I STOP your cells from building their mitotic spindles.
When I walk in, mitosis freezes in its tracks.
PHASE SPECIFICITY
🩷 M-phase
Memory: “VinBLASt jumps in and BLASTS mitosis before it starts.”
🌿 Green Flags
IV only
Works well in lymphomas/testicular cancer
A classic king
🚩 Red Flags (ADRs)
1) Myelosuppression (THE WORST of all vincas)
🌸 MEMORY HOOK:
👉 VinBLASt = BLASTS the bone marrow
You will never confuse this again.
2) Neuropathy (mild compared to vincristine)
3) Bronchospasm
👉 "When he BLASTS your lungs."
4) DEADLY if given intrathecally
👉 “BLAST = BLASTS your brain = death.”
💔 Resistance
↑ P-gp / MRP drug pumps
👉 Cancer literally "blasts" him back out
💘 2) VinCRISTine — “CRISPS Your Nerves”
📍 29 • Vinca Alkaloid • M-phase Chaos Maker
About Me (MOA)
Same MOA as vinblastine:
I block microtubule polymerization, stopping mitosis.
PHASE SPECIFICITY
💅 M-phase
🌿 Green Flags
Classic for pediatric cancers + lymphomas
IV only
🚩 Red Flags (ADRs)
THIS is the KEY difference!
🔥 1) SEVERE peripheral neuropathy
✨ MEMORY HOOK:
👉 VinCRISTine = CRISPS the nerves
Think: CRISPY WIRES, CRISPY NERVES
(Numbness, tingling, foot drop, etc.)
🔥 2) Minimal myelosuppression
Opposite of vinblastine
👉 “CRISTine is too busy crisping nerves to blast the marrow.”
🔥 3) DEADLY if intrathecal
Same danger.
NEVER IT.
💔 Resistance
↑ P-gp / MRP
(The usual)
💘 3) Paclitaxel — “The Overprotective Lover Who FREEZES You in Place”
📍 35 • Taxane • M-phase Stabilizer
About Me (MOA)
I stabilize microtubules so tightly that they can’t move.
Cells get frozen in metaphase — stuck like a toxic situationship.
PHASE SPECIFICITY
💗 M-phase
🌿 Green Flags
IV or intraperitoneal
Used in breast, ovarian, lung cancers
Iconic
🚩 Red Flags (ADRs)
❄ 1) Peripheral neuropathy
👉 “He TAXES your nerves until they freeze.”
💉 2) Myelosuppression
🎀 3) Hypersensitivity reactions
→ Due to Cremophor EL vehicle
👉 “He’s allergic to commitment AND everything else.”
❤ 4) Bradycardia + hypotension
👉 “Your heart slows when he’s around.”
💔 Resistance
↑ P-gp
👉 “He gets TAXED out of the cell.”
💘 4) Docetaxel — “Doctor Taxel: Hotter, Stronger, but Makes You SOB”
📍 38 • Stronger Taxane • M-phase Arrest Expert
About Me (MOA)
Same MOA as paclitaxel:
→ Stabilizes microtubules with EVEN HIGHER affinity
PHASE SPECIFICITY
✨ M-phase
🌿 Green Flags
Only IV
Standard in prostate + breast cancer
More potent binding = more drama
🚩 Red Flags (ADRs)
🫁 1) Pulmonary toxicity
👉 “DOCetaxel = DOCTOR for lung issues because he CAUSES them.”
🩸 2) Myelosuppression
(Worse than paclitaxel)
🧬 3) Large interpatient variability (CYP3A4)
👉 “You need a DOCTOR to figure out your dose.”
💔 Resistance
↑ P-gp → same as paclitaxel
🌋 ALKYLATING AGENTS — NITROGEN MUSTARDS
(Memory: they ALL covalently bind DNA, causing crosslinks → apoptosis.
All cause secondary malignancies because they're DNA-damaging kings.)
💘 1) Cyclophosphamide — “The Party Animal with the TOXIC Pee”
📍 Age 40+ • CYP2B6 F-Boy • DNA Crosslinker
About Me (MOA)
I’m a prodrug activated by CYP2B6 → form alkylating metabolites that crosslink DNA.
✨ Memory: Cyclo = cycle through the liver → activated.
🌿 Green Flags
Oral or IV
Works in everything (lymphoma, breast cancer, autoimmune diseases)
🚩 Red Flags (ADRs)
🔥 1) Hemorrhagic cystitis
CAUSE: my metabolite acrolein
🥤 Memory hook: “Cyclo makes you CYCLE TO THE BATHROOM.”
→ MUST pair me with MESNA (my babysitter)
🔥 2) Bone marrow suppression
Big time. I'm toxic like that.
🔥 3) Neurotoxicity
🔥 4) Cardiotoxicity (HIGH DOSE)
→ “Cyclo’s heart breaks PEOPLE, not the other way around.”
🔥 5) HIGH emetogenicity
→ "Cycle-throw-up-phamide."
🔥 6) SECONDARY cancers
Especially bladder + blood cancers.
💔 Resistance Mechanisms
Super high-yield — and we’re making them MEMORABLE:
1) ↑ Glutathione conjugation
👉 Cancer detoxes him like a green smoothie.
2) ↑ Aldehyde dehydrogenase metabolism
👉 Cancers become “sober queens” and break him down faster.
3) ↑ MGMT DNA repair
👉 “Clean-up crew fixes Cyclo’s damage.”
💘 2) Ifosfamide — “Cyclophosphamide’s Messier, Hotter Brother”
📍 CYP3A4 player • DNA Crosslinker • Chaos energy
About Me
I’m similar to cyclophosphamide but:
👉 Activated mainly by CYP3A4
👉 More neurotoxicity
👉 Still causes hemorrhagic cystitis
👉 STILL needs mesna (mandatory babysitter)
👉 SAME resistance mechanisms
📌 Memory:
“Ifosfamide = IFO-SHAMED cyclophosphamide (more toxic).”
IFOS = I-FOS → I F** UP YOUR CNS.*
🚩 ADRs
🔥 1) Hemorrhagic cystitis
→ NEED mesna
Memory: Ifosfamide = “If only I had MESNA…”
🔥 2) WORSE neurotoxicity (encephalopathy)
→ Confusion, hallucinations
Memory: “Ifos makes your brain say IF ONLY I WAS OKAY.”
🔥 3) Bone marrow suppression
🚩 SAME RESISTANCE AS CYCLOPHOSPHAMIDE
↑ Glutathione
↑ Aldehyde dehydrogenase
↑ MGMT
💘 3) MESNA — “The UTI-Free Gentleman”
📍 Supportive King • Loves Bladders
About Me (MOA)
I bind acrolein, the toxic bladder metabolite from cyclophosphamide + ifosfamide.
Memory:
MESNA = MI SAYS NO to ACROLEIN.
🌿 Green Flags
Prevents hemorrhagic cystitis
50% oral bioavailability
(Memory: “MESNA is half committed.”)
🚫 Red Flags
None. He’s literally perfect.
🌈 PLATINUM AGENTS — THE ‘HEAVY METAL BOYFRIENDS’
MOA for ALL:
→ DNA crosslinking (intra + inter-strand)
→ Bind N7 of guanine
→ Cell can’t replicate
ALL can cause peripheral neuropathy, but differently.
ALL have platinum-like nausea (emetogenicity varies).
💘 4) Cisplatin — “Mr. Vomit + Kidney Slayer”
📍 OG Platinum Daddy • DNA Crosslinker • High Emetic Energy
About Me (MOA)
Activated by hydrolysis → binds N7 guanine → forms crosslinks → kills DNA.
🚩 ADRs you MUST know
🔥 1) NEPHROTOXICITY (MAJOR)
Irreversible.
“Cisplatin = CISTHEKIDNEYS”
🔥 2) Ototoxicity (cumulative, irreversible)
High-yield AF.
🔥 3) Highly emetogenic
Like… THE WORST.
Memory: “CIS = SICK.”
🔥 4) Myelosuppression (less severe than carboplatin)
💔 Resistance
Three ways cancers escape him:
↓ intracellular drug uptake (↓ CTR1)
↑ glutathione / thiol inactivation
↑ NER (nucleotide excision repair)
Memory:
Cisplatin fights DNA → cancer hires REPAIRMEN & SECURITY GUARDS.
💘 5) Carboplatin — “Softer, Sweeter, But Still Toxic”
📍 Cisplatin’s nicer cousin
MOA
Same as cisplatin → hydrolysis → DNA crosslinks.
🚩 ADRs
🔥 1) Myelosuppression (WORSE than cisplatin)
Memory: “CARBOpLATIN → crushes the BONE marrow.”
🔥 2) Moderate–high emetogenicity
Less than cisplatin.
🔥 3) MUCH less nephrotoxic + ototoxic
Used when kidneys are fragile.
❤ Resistance
Identical to cisplatin.
💘 6) Oxaliplatin — “The Cold, Emotionally Unavailable King”
📍 DNA Crosslinker • Arctic Energy
MOA
Same as others → hydrolysis → DNA adducts.
🚩 ADRs
❄ 1) Peripheral sensory neuropathy
→ Triggered or worsened by cold exposure
Memory:
OXALI = “OH IT’S COLD.”
Students NEVER forget this again.
❄ 2) Anemia
⭐LESS emetogenic than cisplatin
❤ Resistance
Same platinum-style resistance.
🌈 SUPER FAST NAME-BASED MEMORY HOOKS
Cyclophosphamide
“CYCLO = cycle to the bathroom” → hemorrhagic cystitis
Needs MESNA
Bone marrow suppression
Cardiotoxicity at high doses
Ifosfamide
“I-FOs your brain” → worst neurotoxicity
Still cystitis → MESNA
Same resistance
MESNA
"MESNA = My pee is safe now."
CISplatin
CIS =
CIS-the-kidneys
CIS-the-ears
CIS-the-stomach (vomit)
CARBOplatin
CARBO = carbs = carbs go to bone
→ bone marrow suppression biggest toxicity
OXALIplatin
OX = oxyGEN → cold wind → cold neuropathy
❤🔥 DATING PROFILES — ANTHRACYCLINES (THE RED FLAGS… LITERALLY)
Memory: Anthracyclines = Red drugs, red hearts, red flags.
💘 1) Doxorubicin — “THE RED FLAG WALKING”
📍 Topo II Seducer • Free Radical Enthusiast • Red Queen
About Me (MOA)
I’m THE classic anthracycline.
I do THREE toxic love languages:
1⃣ Bind Topo II + DNA → form a toxic tripartite complex
2⃣ Intercalate into DNA (slide between base pairs like I own the place)
3⃣ Create free radicals → oxidative damage
MEMORY:
💋 “Doxo = DOX your heart, DOX your DNA, DOX your mitochondria.”
🌹 Green Flags
IV bolus
Treats a ton of cancers
Red and sexy
💔 Red Flags (ADRs)
❤ 1) CARDIOTOXICITY (DOSE-LIMITING)
→ Congestive heart failure
→ Due to free radicals
→ WORSE at high cumulative doses
MEMORY:
💔 “Doxo DOX-es your heart.”
🩸 2) Myelosuppression
🤢 3) High–moderate emetogenicity
💅 Bonus:
Dexrazoxane = his toxic relationship therapist
→ Reduces cardiotoxicity
→ “Dexo needs Dexrazoxane to behave.”
💔 Resistance Mechanisms
↑ P-gp efflux
→ “Doxo gets kicked OUT of the relationship.”↓ Topo II activity
→ “No target, no drama.”↑ Glutathione peroxidase
→ “Cancer detoxes his free radicals.”
💘 2) Epirubicin — “Doxo’s Chill Twin with Slightly Less Heartbreak”
📍 Topo II Queen #2 • Red but Less Toxic
About Me
Basically DOXO but smoother.
Same 3-part MOA:
Topo II poisoning
Intercalation
Free radicals
💔 ADRs
Myelosuppression
Cardiotoxicity (still there)
High–moderate emetogenicity
But less cardiotoxic than doxorubicin.
MEMORY:
💓 EPI-rubicin = EPI-pen for the heart → slightly safer.
💔 Resistance
Same as doxo.
💘✨ PARP INHIBITORS — THE “BREAK-UP SPECIALISTS”
Memory:
🧬 These target BER (base excision repair) → cause ssDNA breaks → turn into double-strand breaks in replication.
They SLAY HR-deficient cancers.
💘 3) Olaparib — “The DNA Breakup Expert”
📍 PARP1/2 Blocker • Single-Strand Homewrecker
About Me (MOA)
I inhibit PARP1 & PARP2, causing:
1⃣ ssDNA breaks not repaired
2⃣ These turn into double-strand breaks during replication
3⃣ HR-deficient cells (like BRCA-mutated) DIE dramatically
MEMORY:
💅 “OLA-parib = OLA I shattered your DNA.”
🌿 Green Flags
Great for BRCA cancers
Oral
Precision medicine queen
💔 Red Flags (ADRs)
Myelosuppression
GI upset
Fatigue
CYP3A4 metabolism → tons of interactions
(“Olaparib NEVER dates someone without checking their medication list.”)
💔 Resistance
↑ P-gp efflux (“OLA gets O-LAUNCHED out”)
Restored HR repair (cancer gets back with its ex DNA)
↑ Replication fork repair
💘 4) Niraparib — “The PARP Inhibitor with ♥ Blood Pressure Issues”
📍 PARP1/2 Blocker • CVS Toxicity Queen
About Me (MOA)
Same as olaparib → PARP inhibition → ssDNA accumulation → lethal DSBs.
🌿 Green Flags
Metabolized by carboxylesterase (NOT CYP3A4 like olaparib!)
Memory: NIRA = NOT CYP.
💔 Red Flags (ADRs)
Myelosuppression
CVS toxicities:
Hypertension
Hypertensive crisis (!!)
MEMORY:
❤🔥 “NIRA-parib = NEARLY gave me a heart attack.”
💔 Resistance
Same trio as olaparib:
↑ drug efflux
restored HR
↑ fork repair
🌈 SUPERFAST SUMMARY (HOW TO NEVER FORGET THEM)
Doxorubicin (DOX your heart)
❤ Cardiotoxicity (dose-dependent)
🧬 Topo II + intercalation + free radicals
💊 Dexrazoxane rescues
Epirubicin (EPI-pen for the heart)
Same MOA, slightly less cardiotoxic
Olaparib (OLA I broke your DNA)
PARP1/2 inhibitor
CYP3A4 metabolism
Myelosuppression
Resistance: P-gp, HR restoration, fork repair
Niraparib (NIRA = NEAR HEART ATTACK)
PARP1/2 inhibitor
Hypertension + hypertensive crisis
Carboxylesterase metabolism
💘✨ DATING PROFILES — SMALL MOLECULE TYROSINE KINASE INHIBITORS (TKIs)
MOA memory: TKIs = BLOCK signal transduction = BLOCK cell survival signals
💗 1) Palbociclib — “The G1/S Blocker Daddy”
📍 CDK4/6 Softboy • Cell Cycle Gatekeeper
About Me (MOA)
I inhibit CDK4/6, which means:
→ I STOP the cell cycle at G1/S
→ No progression
→ No replication
→ Apoptosis
→ “No one gets through the gate without my permission.”
MEMORY:
📌 PALBO = PAUSE BUTTON at G1/S.
🌿 Green Flags
Oral
Predictable PK
Works beautifully in HR+/HER2– breast cancer
💔 Red Flags (ADRs)
💥 Myelosuppression
(He depletes your WBCs like he depletes your emotional capacity 😭)
🧬 Resistance
Loss of Rb → If there’s no Rb, Palbo can’t stop E2F.
Cyclin E overexpression → Cell cycle GO brrrr
E2F amplification → Too much signal
↑ ABC-transporter efflux → “BYE PALBO” 🚪
💗 2) Ribociclib — “Palbo’s Hot Sister With Heart Issues”
📍 CDK4/6 Baddie • Known for QT drama
About Me (MOA)
Same as Palbo → CDK4/6 inhibitor, G1/S arrest
💔 Red Flags
Myelosuppression
QT prolongation 💔
→ "Ribo makes your HEART skip a beat… literally."
MEMORY:
📌 RIBO → RIBBON ECG → QT prolongation.
🧬 Resistance
Same as Palbo.
They’re twins.
💗 3) Abemaciclib — “The Diarrhea Demon”
📍 CDK4/6 Queen • Runs the Cell Cycle AND Your Bowels
MOA
Same as Palbo + Ribo → CDK4/6 inhibition → G1/S arrest.
💔 Red Flags
Myelosuppression
DIARRHEA (SEVERE)
→ “ABE-MA-SHITS.”
MEMORY:
💩 ABE → ABOOM.
🧬 Resistance
Same as Palbo + Ribo
Loss of Rb
Cyclin E issues
Efflux pumps, etc.
🔥 4) Imatinib — “The ORIGINAL TKI Daddy”
📍 BCR-Abl Slayer • Miracle Worker • Chronic Myeloid Leukemia King
About Me (MOA)
I specifically inhibit BCR-Abl TK —
the fusion oncoprotein in CML.
→ Block ATP-binding
→ Prevent phosphorylation
→ Stop proliferation
MEMORY:
📌 IMATINIB = I-MATCH-INHIBITS BCR-ABL.
🌿 Green Flags
Oral
Targeted therapy pioneer
Made CML into a chronic manageable disease 💅
💔 Red Flags (ADRs)
Myelosuppression
Edema (especially periorbital → puffy eyes)
Hepatic toxicity
MEMORY:
😳 “IMATINIB MAKES YOU IMMA-TINY because of swelling.”
🧬 Resistance
TK domain mutations, especially T315I mutation
→ NO TKI except PONATINIB works here.BCR-Abl amplification
↑ Drug efflux
💗 5) Gefitinib — “The EGFR Mutant Lover With GI Problems”
📍 EGFR Exon19/L858R Specialist • ATP Site Homewrecker
About Me (MOA)
I competitively inhibit the ATP-binding site of EGFR-TK.
I work BEST in cancers with:
✔ Exon 19 deletion
✔ L858R mutation
MEMORY:
🌸 GEFITINIB = GET-FIT-IN-IB (fits into ATP-binding pocket).
🌿 Green Flags
Oral
Great for EGFR-mutated NSCLC
💔 Red Flags (ADRs)
Diarrhea
Nausea/vomiting
QT prolongation
Rash (classic EGFR inhibitor class effect)
🧬 Resistance
KRAS or NRAS mutations
HER1-TK T790M mutation (very high yield!)
↑ drug efflux
MEMORY:
📌 T790M = the “THIS relationship is over” mutation.
🌈 SUPERFAST SUMMARY CARD (never forget this)
CDK4/6 inhibitors (Palbo, Ribo, Abe)
MOA → G1/S arrest
Class toxicity → MYELOSUPPRESSION
Ribo → QT prolongation
Abe → diarrhea
Resistance → loss of Rb, cyclin E, E2F amplification, ABC efflux
Imatinib
MOA → inhibits BCR-Abl
ADR → edema, liver issues, myelosuppression
Resistance → TK mutations (esp. T315I)
Gefitinib
MOA → inhibits EGFR-TK (ATP-binding site)
ADR → diarrhea, rash, QT prolongation
Resistance → KRAS mutations, T790M mutation
💘✨ DATING PROFILES — SMALL MOLECULE TYROSINE KINASE INHIBITORS (TKIs)
MOA memory: TKIs = BLOCK signal transduction = BLOCK cell survival signals
💗 1) Palbociclib — “The G1/S Blocker Daddy”
📍 CDK4/6 Softboy • Cell Cycle Gatekeeper
About Me (MOA)
I inhibit CDK4/6, which means:
→ I STOP the cell cycle at G1/S
→ No progression
→ No replication
→ Apoptosis
→ “No one gets through the gate without my permission.”
MEMORY:
📌 PALBO = PAUSE BUTTON at G1/S.
🌿 Green Flags
Oral
Predictable PK
Works beautifully in HR+/HER2– breast cancer
💔 Red Flags (ADRs)
💥 Myelosuppression
(He depletes your WBCs like he depletes your emotional capacity 😭)
🧬 Resistance
Loss of Rb → If there’s no Rb, Palbo can’t stop E2F.
Cyclin E overexpression → Cell cycle GO brrrr
E2F amplification → Too much signal
↑ ABC-transporter efflux → “BYE PALBO” 🚪
💗 2) Ribociclib — “Palbo’s Hot Sister With Heart Issues”
📍 CDK4/6 Baddie • Known for QT drama
About Me (MOA)
Same as Palbo → CDK4/6 inhibitor, G1/S arrest
💔 Red Flags
Myelosuppression
QT prolongation 💔
→ "Ribo makes your HEART skip a beat… literally."
MEMORY:
📌 RIBO → RIBBON ECG → QT prolongation.
🧬 Resistance
Same as Palbo.
They’re twins.
💗 3) Abemaciclib — “The Diarrhea Demon”
📍 CDK4/6 Queen • Runs the Cell Cycle AND Your Bowels
MOA
Same as Palbo + Ribo → CDK4/6 inhibition → G1/S arrest.
💔 Red Flags
Myelosuppression
DIARRHEA (SEVERE)
→ “ABE-MA-SHITS.”
MEMORY:
💩 ABE → ABOOM.
🧬 Resistance
Same as Palbo + Ribo
Loss of Rb
Cyclin E issues
Efflux pumps, etc.
🔥 4) Imatinib — “The ORIGINAL TKI Daddy”
📍 BCR-Abl Slayer • Miracle Worker • Chronic Myeloid Leukemia King
About Me (MOA)
I specifically inhibit BCR-Abl TK —
the fusion oncoprotein in CML.
→ Block ATP-binding
→ Prevent phosphorylation
→ Stop proliferation
MEMORY:
📌 IMATINIB = I-MATCH-INHIBITS BCR-ABL.
🌿 Green Flags
Oral
Targeted therapy pioneer
Made CML into a chronic manageable disease 💅
💔 Red Flags (ADRs)
Myelosuppression
Edema (especially periorbital → puffy eyes)
Hepatic toxicity
MEMORY:
😳 “IMATINIB MAKES YOU IMMA-TINY because of swelling.”
🧬 Resistance
TK domain mutations, especially T315I mutation
→ NO TKI except PONATINIB works here.BCR-Abl amplification
↑ Drug efflux
💗 5) Gefitinib — “The EGFR Mutant Lover With GI Problems”
📍 EGFR Exon19/L858R Specialist • ATP Site Homewrecker
About Me (MOA)
I competitively inhibit the ATP-binding site of EGFR-TK.
I work BEST in cancers with:
✔ Exon 19 deletion
✔ L858R mutation
MEMORY:
🌸 GEFITINIB = GET-FIT-IN-IB (fits into ATP-binding pocket).
🌿 Green Flags
Oral
Great for EGFR-mutated NSCLC
💔 Red Flags (ADRs)
Diarrhea
Nausea/vomiting
QT prolongation
Rash (classic EGFR inhibitor class effect)
🧬 Resistance
KRAS or NRAS mutations
HER1-TK T790M mutation (very high yield!)
↑ drug efflux
MEMORY:
📌 T790M = the “THIS relationship is over” mutation.
🌈 SUPERFAST SUMMARY CARD (never forget this)
CDK4/6 inhibitors (Palbo, Ribo, Abe)
MOA → G1/S arrest
Class toxicity → MYELOSUPPRESSION
Ribo → QT prolongation
Abe → diarrhea
Resistance → loss of Rb, cyclin E, E2F amplification, ABC efflux
Imatinib
MOA → inhibits BCR-Abl
ADR → edema, liver issues, myelosuppression
Resistance → TK mutations (esp. T315I)
Gefitinib
MOA → inhibits EGFR-TK (ATP-binding site)
ADR → diarrhea, rash, QT prolongation
Resistance → KRAS mutations, T790M mutation
.
💘✨ DATING PROFILES — EGFR & HER2 & VEGF MONOCLONAL ANTIBODIES
💗 1) Cetuximab — “The Chimeric King With Attitude (and Acne)”
📍 IgG1 Chimeric • EGFR Blocker • Drama Magnet
💋 About Me (MOA)
I’m a chimeric IgG1 monoclonal antibody targeting EGFR (HER1).
My love languages:
1⃣ Block ligand → receptor activation
2⃣ Induce complement-mediated cytotoxicity (CDC)
3⃣ Shut DOWN EGFR signaling pathways
4⃣ Make cancer cells BREAK UP with proliferation 😌
MEMORY:
🐆 “CETUXIMAB = CHIMERIC”
Think Cheetah for “CETUX”— spotted → acne rash.
🌿 Green Flags
IV infusion
Works खास in EGFR-dependent colorectal cancer
ADCC + CDC effects
💔 Red Flags (ADRs)
🛑 Acne-like rash (super classic)
🛑 Infusion reactions
🛑 Hypomagnesemia
Memory:
“If you DATE CETUXIMAB, you will BREAK OUT.”
🧬 Resistance / Biomarker Notes
↑ EGFR copy number (cancer becomes obsessed with EGFR)
Switch to HER2 pathway
KRAS or BRAF mutations = DO NOT USE
(if KRAS is mutated → MAPK pathway is ON anyway)
Memory:
🔥 CETUXIMAB only dates cancers with NORMAL KRAS.
💗 2) Panitumumab — “The Calm, Fully Human, Low-Drama Sister”
📍 IgG2 Fully Human • EGFR Blocker • Soft Girl
💋 About Me (MOA)
Same target as cetuximab → EGFR/HER1
BUT I’m fully human (IgG2) so:
→ Fewer infusion reactions
→ More predictable PK
→ Still works best in KRAS wild-type
🌿 Green Flags
IV
Fewer hypersensitivity reactions vs cetux
Same anti-EGFR activity
💔 Red Flags (ADRs)
Acneiform rash
Diarrhea
Hypomagnesemia
🧬 Resistance
Same as cetuximab:
KRAS or BRAF mutations
HER2 pathway compensation
EGFR amplification
MEMORY:
🧍♀ Pani-tumumab = “PANIc if KRAS is mutated — drug won’t work.”
💗 3) Trastuzumab — “HER2’s Toxic Lover With Heart Problems”
📍 IgG1 Humanized • HER2 Blocker • Breaks Hearts (Literally)
💋 About Me (MOA)
I am THE HER2 monoclonal antibody.
I bind the extracellular domain of HER2 and:
→ Block dimerization
→ Promote receptor internalization
→ Encourage immune-mediated killing
→ Slow down HER2+ tumor proliferation
MEMORY:
💗 “TRASTUZUMAB = TRUST ME, BUT I’LL BREAK YOUR HEART.”
🌿 Green Flags
IV
Life-changing for HER2+ breast cancer
Synergistic with taxanes
💔 Red Flags (ADRs)
❤ CARDIOMYOPATHY (major exam classic!)
Even worse combined with anthracyclines (doxo, epi)
Reversible (unlike doxorubicin)
Memory:
💔 HER2 → HEART TOO
TRASTUZUMAB → TRASTU-heart-MAB
🧬 Resistance
↑ EGFR-dependent signaling
HER2 truncations
Activation of downstream pathways (PI3K, MAPK)
💗 4) Bevacizumab — “The No-Blood-Vessel Boyfriend”
📍 IgG1 Anti-VEGF • Angiogenesis Blocker • GI-Crisis King
💋 About Me (MOA)
I bind VEGF-A, preventing it from activating VEGFR on endothelial cells.
This means:
🚫 No angiogenesis
🚫 No new blood vessels
🚫 Tumor starves
🚫 Lower metastasis potential
MEMORY:
🌿 “BEVA = Be Very Anti-angiogenesis.”
🌿 Green Flags
IV infusion
Works in colorectal cancer, lung cancer, renal cell cancer
Great combo with chemotherapy
💔 Red Flags (ADRs)
⚡ Hypertension (dose-dependent)
⚡ Hemorrhage
⚡ GI perforation
⚡ Thromboembolism
⚡ Delayed wound healing
MEMORY:
🩸 “Bevacizumab doesn’t let anything grow… not even your GI tract integrity.”
🧬 Resistance
Cancer activates alternative angiogenesis pathways (FGF, PDGF)
VEGF gene upregulation
MEMORY:
🌱 “If VEGF is blocked, cancer plants NEW VEGFs.”
🌈✨ QUICK MEMORY VIBES (AESTHETIC EDITION)
Cetuximab → CHIMERIC (IgG1), acne rash, KRAS wild-type only
🐆 Cheetah → Spots → Rash
Panitumumab → Fully human (IgG2), same rash, fewer reactions
🧍♀ Soft girl EGFR antibody
Trastuzumab → HER2 blocker, CARDIOTOXICITY
💗 “Trust me, but I’ll break your heart.”
Bevacizumab → Anti-VEGF, hypertension, hemorrhage, GI perforation
🌿 “BE VERY anti-angiogenesis.”
❤🔥 IMMUNE CHECKPOINT INHIBITOR DATING PROFILES
(aesthetic, chaotic, ultra high-yield)
💘 1) Ipilimumab — “The CTLA-4 Warrior Queen (IgG1)”
📍 Fully Humanized • IgG1 • CTLA-4 Blocker • T-Cell Activator
💋 About Me (MOA)
I bind CTLA-4, the OG brake on T-cells.
→ CTLA-4 sits on T-cells
→ It normally stops activation
→ I BLOCK IT
→ T-cells go FERAL and attack tumors
→ And also sometimes your own organs (oopsie 😭)
MEMORY HOOKS:
🔥 IPI = IP-UNLEASHES T-cells
🔥 CTLA-4 = “Cease This Lymphocyte Activation” → I REMOVE THE CEASE.
🧬 Origin / Type
Fully humanized
IgG1
REMEMBER:
📌 Only IPI = IgG1 AND CTLA-4
Everything else is PD–something.
💔 ADRs (Classic!)
→ Skin reactions (rash, pruritus)
→ Colitis
→ Hepatitis
→ Basically: “immune system goes berserk”
Memory:
💥 “IPI = I PEE FIRE FROM COLITIS.”
🧬 Resistance
Tumor loses IFN-γ signaling
Reduced neoantigen presentation
Altered tumor microenvironment
Upregulation of other checkpoints
💘 2) Nivolumab — “The Chill PD-1 Boyfriend (IgG4)”
📍 Fully Humanized • IgG4 • PD-1 Blocker
💋 About Me (MOA)
I block PD-1 on T-cells & immune cells,
which normally tells T-cells:
🛑 “Stop attacking, sweetie.”
I REMOVE that signal →
T-cells resume killing cancer.
MEMORY:
🫶 NIVO = “NO VOICE MAIL for PD-1.” (I ignore PD-1’s stop signal.)
🧬 Origin / Type
Fully humanized
IgG4 (very important!)
PD-1 = IgG4 gang (Nivo + Pembro)
💔 ADRs
Skin toxicity
Pneumonitis
Hepatitis
Thyroiditis
Colitis
(“Basically pick a body organ and inflame it” 😭)
🧬 Resistance
Same general immune escape:
↓ antigen presentation
↑ alternate checkpoint pathways
Mutations in IFN-γ genes
💘 3) Pembrolizumab — “PD-1 Daddy With the PROFOUND Infusion Drama”
📍 Fully Humanized • IgG4 • PD-1 Blocker
💋 About Me
SAME MOA as nivolumab:
→ Bind PD-1 on T-cells
→ Release immune brakes
→ Immune system goes SUPER SAIYAN
🧬 Origin / Type
Fully humanized
IgG4
Same as Nivolumab
💔 ADRs
→ Same irAEs as Nivo
BUT
🚨 More infusion-related reactions
Memory:
💅 PEMBRO = “PREPARE BRO… infusion drama.”
🌈 SO HOW TO REMEMBER PD-1 AGENTS?
🟪 PD-1 = IgG4 (Nivo, Pembro)
🟪 Target lives on T-cells & immune cells
🟪 MOA = Unleash T-cells
🟪 infusion drama = Pembro
🟪 Nivo is the chill one
💘 4) Atezolizumab — “The Bougie PD-L1 Baddie Who BLOCKS Tumor Ghosting”
📍 Fully Humanized • IgG1 • PD-L1 Blocker
💋 About Me (MOA)
I block PD-L1, which is:
→ Found on tumor cells
→ And on normal immune and tissue cells
Tumors use PD-L1 to GHOST T-cells
(“lol no kill me, I have PD-L1 🥺”)
I BLOCK that signal →
T-cells SURGE back and destroy tumors.
MEMORY:
✨ Atezo = “A-TAY-ZO no ghosting allowed.”
✨ PD-L1 = L for Liar → tumor lies to T-cells.
🧬 Origin / Type
Fully humanized
IgG1
💔 ADRs
Typical irAEs (colitis, pneumonitis, hepatitis)
Infusion reactions
💘 5) Avelumab — “The HUMAN PD-L1 Sweetheart With ADCC Powers”
📍 Fully Human • IgG1 • PD-L1 Blocker
💋 MOA
Same as Atezolizumab → PD-L1 blocker
BUT
I still have Fc activity → can trigger ADCC (unlike IgG4)
🧬 Origin / Type
Fully human
IgG1
Memory:
🌸 AVE = AVENUE of HUMANITY
Only PD-L1 drug that is FULLY HUMAN!!
💔 ADRs
Fever
Infusion reactions
irAEs (pneumonitis, colitis)
💘 6) Durvalumab — “The Human PD-L1 Mom Who Doesn’t Take No for an Answer”
📍 Fully Human • IgG1 • PD-L1 Blocker
💋 MOA
Same as other PD-L1 inhibitors.
🧬 Origin / Type
Fully human
IgG1
💔 ADRs
Immune-related reactions
Infusion reactions
🌈✨ ULTRA HIGH-YIELD COMPARISON TABLE (YOU WILL NEVER MIX THESE AGAIN)
Drug | Target | Where Target Lives | IgG Type | Humanized? | Key ADR |
|---|---|---|---|---|---|
Ipilimumab | CTLA-4 | T-cells | IgG1 | Fully humanized | Skin rash, colitis |
Nivolumab | PD-1 | T-cells + immune cells | IgG4 | Fully humanized | irAEs |
Pembrolizumab | PD-1 | T-cells + immune cells | IgG4 | Fully humanized | Infusion reactions |
Atezolizumab | PD-L1 | Tumor cells | IgG1 | Fully humanized | irAEs |
Avelumab | PD-L1 | Tumor cells | IgG1 | Fully human (not just humanized!) | ADCC |
Durvalumab | PD-L1 | Tumor cells | IgG1 | Fully human | Pneumonitis, colitis |
🌟 EASY MEMORY HACKS
🌸 CTLA-4 = Ipi
Only CTLA-4 drug in the whole group
IgG1
Found on T-cells
Causes WORST colitis
🌸 PD-1 = Nivo + Pembro (“the -mab siblings”)
BOTH IgG4
BOTH fully humanized
BOTH found on T-cells
Pembro = infusion drama
Nivo = chill
🌸 PD-L1 = Atezo, Avelu, Durva (“the A-team”)
ALL IgG1
ALL infusion reactions
ALL irAEs
Avelumab = ONLY one that is fully human1
SUMMARY
🌸 ANTIMETABOLITES (Pink Block)
Methotrexate → DHFR blocker (S-phase) → myelosuppression + nephrotox → rescued by leucovorin.
Ralitrexed —> Competitive TS inhibition via polyglutamation —> IV
5-FU → TS ternary complex “suicide trap” → hand–foot syndrome → boosted by leucovorin.
Capecitabine → Oral 5-FU → same effects → hand–foot syndrome.
Cytarabine (Ara-C) → Cytidine analog —> DNA chain terminator (S-phase) → cerebellar + ocular toxicity → IT/IV.
Gemcitabine → Cytidine analog —> Chain terminator → Hemolytic Uremic Syndrome + myelosuppression → potent radiosensitizer.
💜 TOPOISOMERASE INHIBITORS (Lavender Block)
Irinotecan → Topo I inhibitor → “I-run-to-the-can” diarrhea (life-threatening) → UGT1A1 matters —> MRP PUMP “More runny poop”
Etoposide → Topo II inhibitor (S/G2) → secondary leukemia → P-gp resistance — heart
💙 MICROTUBULE AGENTS (Baby Blue Block)
Vincristine → Prevents MT formation → severe neuropathy → NEVER IT (fatal).
Vinblastine → Same MOA → myelosuppression > neuropathy → NEVER IT.
Paclitaxel → Stabilizes MT (M-phase freeze) → hypersensitivity + neuropathy → premedicate.
Docetaxel → Same but stronger binding → pulm tox + fluid retention → CYP3A4 variability.
🌿 ALKYLATING AGENTS
Cyclophosphamide → DNA alkylator → hemorrhagic cystitis → MESNA required.
Ifosfamide → DNA crosslinker → neurotoxicity + cystitis → MESNA required.
Mesna —> Prevention of hemorrhagic cystitis by reacting with acrolein
🍓 PLATINUM AGENTS
Cisplatin → Inter + intrastrand DNA crosslinking ; N7 of guanine → nephrotox, ototox, MOST emetogenic.
Carboplatin → Same target → myelosuppression (dose-limiting).
Oxaliplatin → Same target → cold-triggered neuropathy.
❤ ANTHRACYCLINES (Rose Block)
Doxorubicin → 1) Topo II DNA Drug triparite complex 2) Intercalcates DNA 3) free radicals → dose-dependent cardiotoxicity → dexrazoxane protects.
Epirubicin → Doxorubicin with slightly altered tox → still cardiotoxic + myelosuppressive.
🌿 PARP INHIBITORS
Olaparib → PARP inhibitor → BRCA-sensitive tumors —> myelosuppression.
Inhibits single sstranded DNA breaks repaired by BER —>
cause damage to double stranded DNA breaks
HR repair deficiency (BER)
Niraparib → PARP inhibitor → HTN + hypertensive crises → monitor BP.
☀ CDK4/6 INHIBITORS (Sunshine Yellow Block)
Palbociclib → CDK4/6 block → G1/s arrest → apoptosis myelosuppression
Ribociclib → Same → QT prolongation (unique red flag).
Abemaciclib → Same → diarrhea (worst of the class).
**ALL Rb; ORALLY ADMINISTERED
🌊 SMALL MOLECULE TKIs (Aqua Block)
Imatinib → BCR-Abl inhibitor → edema + hepatotoxicity → resistant w/ T315I mutation. give ponatinib
Gefitinib → EGFR ATP blocker → rash + diarrhea
works best in exon19del/L858R.
resistance = HER-1 TK mutations T790M
💜 EGFR / HER-1 (Lilac Block)
Cetuximab (IgG1 chimeric; HER-1) → Anti-EGFR → acneiform rash → only works if KRAS wild-type.
Panitumumab (IgG2 human; HER-1) → Anti-EGFR → rash → KRAS WT required → lower infusion reactions.
HER2 / VEGF MABS
Trastuzumab (IgG1 humanized; HER-2) → Anti-HER2 → cardiomyopathy → avoid w/ anthracyclines.
Bevacizumab (IgG1-Anti VEGF) → Inhibition of angiogenesis→ GI perforation + hypertension.
🌈 IMMUNE CHECKPOINT INHIBITORS (Rainbow Block)
Ipilimumab —> (IgG1) → Anti-CTLA4
Nivolumab —> (IgG4) → Anti-PD1
Pembrolizumab —> (IgG4) → Anti-PD1 (SEVERE INFUSION REACTIONS)
Atezolizumab —> (IgG1) → Anti-PDL1 → irAEs.
Avelumab —> (IgG1 fully human) → Anti-PDL1
Durvalumab —> (IgG1 fully human) → Anti-PDL1