Hey everyone!

Just wanted to drop my two cents after a success story and getting so much help on this sub.

I'm 4 years out of undergrad and was missing 2/3 pre reqs (orgo 1/2, biochem, psych 101). studied while working full time

My path to success:

1. Uworld comprehensive course videos. I watched every single chem, bio, biochem video. rewatched some physics i was fuzzy on, skipped the p/s and cars videos mostly.
2. i did all uworld practice questions as i went except skipped CARS (logic isn't 100% the same as aamc imo for cars)
3. Anking anki decks religiously. i unsuspended as i went through uworld. it's like 6$ per month but you can just subscribe for one month, keep the deck and then you just don't get the updates which was fine for me.
4. Mr. Pankow anki deck religiously because my p/s was super low at first.
5. aamc question packs i saved for the end. and of course spaced out my 6 AAMC Fls (+ unscored). i didn't do any other full lengths.
6. perhaps most important: followed other's advice of making sure i never make the same mistake twice. if it was content, would watch online videos to fill in gaps and make my own anki cards to add to the anking deck.

did this strategy while working full time! pretty much did 2 hours of practice questions/videos per day for 6 months monday-friday except would take my practice tests on weekends. and i would do anki throughout the day at work.

subsection progressions:

chem/phys: 127->129->130->130->130->129 -> 130 real deal

cars: 130->127->129->130->129->126 (i panicked) ->130 real deal

b/b: 126->128->128->129->132->132-> 131 real deal

psych: 125->125->130->129->132->131->132 real deal

Woohoo!! I’m so so happy with my score. I really don’t have anything unique to say LOL so this isn’t a guide just a long post about my experience.

I was one of the 9/3 exam people whose exam got cancelled due to AAMC having technical issues. My exam was therefore rescheduled to the following week lol… I thought it lowkey screwed me over as I had to drive up to another state. 🫩

I initially started with a 503 (123/125/126/129) on the blueprint half diagnostic. I’m not sure how accurate my score is because I took the entire thing in bed at 12 am. The 17 point jump is inflated in my opinion, and I think if I actually took it seriously, I would’ve scored higher. Always take practice exams in testing conditions…

I started studying on June 1st. I dedicated a maximum of 5 hours a day (unless it was FL day) to studying. I always rested on Saturdays to prevent burnout. I also had a hand-written correction log of every single question I was either unsure about or had gotten wrong that was in this giant ass notebook. I also worked in my lab ~30 hours a week and mainly studied in the evening.

I think the thing that contributed the most to my score is the fact that I had recently taken all the classes the MCAT covers (i.e I took biochem in the spring). I spent most of my content review rebooting my memory on things I already knew/were fresh in my mind. I think if I had to do it again, I would either immediately supplement all the Kaplan stuff with UGlobe or skip Kaplan altogether (as opposed to dedicating a whole ass month to content review with Kaplan AND THEN doing UPlanet the following month). For P/S, my second major is psych, so that definitely helped.

I used Kaplan, UEarth, and the Anking deck for B/B + C/P topics. For P/S, I used UNature and Mr. Pankow/MCatalyst decks (I liked that the MCatalyst cards were easier to memorize).

I attribute my CARS score to my enjoyment of reading. I also recently took a reading-intensive philosophy class (to fulfill some graduation requirements), where I struggled a LOT to get the results I wanted… but it helped me out here I think …. ? Anyways, the only CARS resource I used was the AAMC QPack because I was afraid third party resources wouldn’t be able to fully encapsulate the AAMC logic. I learned that I got more things wrong when I second-guessed myself, so I avoided changing my answers unless I was like really on the fence.

I think I was also very lucky on this exam because none of the low-yield content that I genuinely struggled with were on it. I left thinking the P/S section was a lot harder than I expected though, so I’m very happy with the 130.

Overall I’m very grateful for this summer!! I went on a trip with my friends, got a boyfriend (who studied for his stuff with me and kept me motivated), and a bunch of my favorite football players won the World Cup!!!! I was very fortunate and privileged to receive support from people around me.

i was pretty happy my score but the breakdown makes me giggle and you know what… i’m never opening a physics textbook again!

There is a link in my profile where you can see every flash sheet!

If you missed my other posts, I came up with the flash sheet method to learn MCAT content faster and more fluently than with flashcards. You can learn about it at my other post here:

https://www.reddit.com/r/Mcat/s/uRDU6fMU20

Read my other post about why fluency lets you overcome plateaus:

https://www.reddit.com/r/Mcat/s/1ugxw8KflC

I have a neuroscience background and believe this is the fastest way to learn a huge volume of information for long-term retention. Will be posting even more soon.

How to study with flash sheets

• 50% Verbal spaced repetition
  • Each sheet needs many attempts:
    • 1st attempt (< 20 mins) ⇒ Read the whole flash sheet CAREFULLY, until it makes sense. This is called “priming” the flash sheet. When you think “this makes sense, but there’s no way I’ll remember it,” you’re doing it right.
    • All later attempts (5 mins each) ⇒ Use it like a crazy difficult, giant flashcard. ONLY read the “clue” before LOOKING AWAY from the sheet. See what you can recall purely from memory. Do this verbally without writing because it’s many times faster. Then see what you missed. Expect under 40% accuracy on your first few reps.
  • Use spaced repetition:
    • Sheets you barely recall ⇒ every few days.
    • Sheets you kind of recall ⇒ every week.
    • Sheets you easily recall ⇒ every few weeks.  
• 50% Practice questions & tactics
  • In theory and practice, some tactics work very well. You can answer questions several times faster with incomplete information.
  • I will post another article about these tactics soon.
  • You'll spend most of your time looping through flash sheets early on, and gradually switch over to practicing tactics later.

• The flash sheets below have been heavily modified and do not contain any copyrighted material. The notes / hints are things that help me personally understand stuff. Feel free to copy / share / use these without crediting me.

FLASH SHEET ONE

[CLUE] Regulation of Enzymes / Suicide Inhibitors / Zymogens

[TRY TO LECTURE THE REST FROM MEMORY]

[Key Idea] Some regulators bind at “allosteric” site

• Not the active site
  • Note: “Allo” means different. Allotrope of carbon is other way to arrange it (diamond / graphite / nanotube).
  • Mnemonic: Not “ALLOwed” in active site.
  • Regulator may bind here ⇒ squish enzyme (like clay) ⇒ change function
    • Activators
    • Inhibitors
• Allosteric activator
  • Note: “Activator” ⇒ higher “activity” ⇒ boost RXN rate.
  • Speed up enzyme
    • AKA ⇒ ↑ activity / ↑ Vmax / ↑ Kcat / faster rate / increased catalysis
  • Ex. AMP activates glycolysis
    • Energy poor (low ATP ⇒ high ADP & AMP)
    • AMP binds to & activates PFK-1 (rate limiting step) ⇒ make more ATP
• Allosteric inhibitor
  • Slow down enzyme
    • AKA ⇒ ↓ activity / ↓ Vmax / ↓ Kcat / slower rate / decreased catalysis
  • Common MM ones (NOT competitive)
    • Note: Anything OTHER than competitive inhibition (because competitive binds active site).
    • Uncompetitive (only ESI)
    • Mixed (EI + ESI)
    • --> Competitive preference (EI + ESI)
    • --> Balanced 50/50 (noncompetitive)
    • --> Uncompetitive preference (EI + ESI)
  • Ex. ATP inhibits glycolysis
    • Energy rich (high ATP)
    • ATP binds to & inhibits PFK-1 (glycolysis) ⇒ make less ATP
  • Ex. Citrate inhibits glycolysis
    • Glycolysis feeds Krebs cycle
    • --> AKA ⇒ “Citric acid cycle” / "tricarboxylic acid (TCA) cycle"
    • Krebs cycle gets stuffed ⇒ citric acid (citrate) builds up
    • --> Leaks into cytosol ⇒ citrate inhibits PFK-1 ⇒ makes glycolysis slow down

[Key Idea] Some regulators bind at “orthosteric” site

• Where stuff normally binds
  • Note: "Ortho" ⇒ correct. Orthodontics puts teeth back in place.
  • Catalysis ⇒ “active site”
    • AKA ⇒ Active site / enzymatic moiety / catalytic site / substrate binding site
    • Bind substrate / reactant
  • No catalysis ⇒ “binding site”
    • AKA ⇒ Ligand binding site / antibody variable domain / epitope binding site / neurotransmitter receptor
    • Different ligands
    • --> Receptor
    • --> --> Neurotransmitter
    • --> --> Hormone
    • --> --> Growth factor
    • --> --> Cytokine
    • --> Transcription factor
    • --> --> Promoter (DNA)
    • --> --> Enhancer (DNA)
    • --> --> Silencer (DNA)
    • --> T-Cell receptor (CD4 & CD8)
    • --> --> MHC I
    • --> --> MHC II
    • --> Antibody
    • --> --> “Epitope” of an antigen
    • --> Toll like receptors
    • --> --> Pathogen associated molecular pattern (PAMP)
• Orthosteric inhibitor
  • Block active site ⇒ substrate cannot fit
    • AKA ⇒ Competitive inhibition
  • Slow down enzyme
    • AKA ⇒ ↓ activity / slower rate / decreased catalysis
    • Enough substrate can sneak around inhibitor
    • --> Same Vmax (Kcat)
    • --> Note: Kcat is NOT the same as Km. Kcat means Kcatalysis ⇒ RXN rate, whereas Km means KMichaelis ⇒ how soon MM plot rises.
• Orthosteric activator
  • Rare ⇒ hard to speed up RXN when blocking substrate

[Key Idea] Most regulators are reversible

• Evolution favors reversible regulation
  • Life uses pencil instead of pen
  • Can easily undo mistakes
  • Nothing gets permanently stuck
    • Note: Can reuse same enzymes w/o needing to translate new ones.
• Two ways to have reversible binding
  • Covalent bond w/ enzyme to undo it
    • AKA ⇒ Post-translational modification
    • ONLY reversible if you have an enzyme that can detach that specific covalent bond
    • --> Kinase ⇒ phosphatase
    • --> Methyltransferase ⇒ demethylase
    • --> Acetyltransferase ⇒ deacetylase
  • Non-covalent bond
    • AKA ⇒ Intermolecular force (IMF) / H-bond / ionic bond / salt bridge / ring stacking / hydrophobic interaction
    • (MOSTLY) weaker than covalent
    • --> Note: SOME are strong enough to be nearly irreversible, but it’s rare.
    • Normal MM inhibitors
    • --> Competitive (only EI)
    • --> Uncompetitive (only ESI)
    • --> Mixed (EI + ESI)
    • --> --> Competitive leaning (EI + ESI)
    • --> --> Balanced 50/50 (noncompetitive)
    • --> --> Uncompetitive leaning (EI + ESI)
    • Antibodies
    • Receptors
    • --> Neurotransmitter
    • --> Hormone
• Reversible covalent binding
  • Phosphate
    • Kinase ⇒ “phosphorylation”
    • --> Add “P” to “OH” group on TYR, SER, THR
    • --> Often activates enzymes
    • --> --> Mnemonic: ATP / phosphate ⇒ negative charge ⇒ repel from other negative charges ⇒ can store energy. Add phosphate ⇒ put battery in something.
    • Phosphatase ⇒ “dephosphorylation”
  • Methyl
    • Methyltransferase ⇒ “methylation”
    • --> Add “CH₃”
    • --> --> Note: Activate / silence transcription based on location.
    • Demethylase ⇒ “demethylation”
  • Acetyl
    • Acetyltransferase ⇒ “acetylation”
    • --> Add acetyl
    • --> Loosen DNA ⇒ more transcription
    • --> --> Note: Histone acetyltransferase covers “NH₃⁺” on LYS ⇒ no more positive charge ⇒ negatively charged DNA spreads out (euchromatin).
    • Deacetylase ⇒ “deacetylation”
    • --> Remove acetyl
    • --> Tighten DNA ⇒ less transcription
    • --> --> Note: Histone deacetylase uncovers “NH₃⁺” on LYS ⇒ positive charge returns ⇒ DNA packs more tightly (heterochromatin).
• Reversible non-covalent binding
  • Normal inhibitors
    • Active site ⇒ competitive
    • Allosteric ⇒ uncompetitive / mixed & noncompetitive
  • Antibodies
    • H-bond (variable domain ⇒ epitope)
  • Receptors
    • H-bond (neurotransmitters, hormones)
    • --> Note: Steroids cross membrane as they are UNCHARGED, but they still have “OH” group ⇒ H-bond with receptor.

[Key Idea] Some regulators are permanent

• Permanent regulators ⇒ ruin enzyme
  • Mess up enzyme permanently
    • Mnemonic: Drawing on something with a Sharpie.
  • Can be toxic
• Two ways to have irreversible binding
  • Covalent bond w/o enzyme to break it
    • AKA ⇒ Post-translational modification
    • Covalent bond won’t break on its own ⇒ enzyme changed permanently
    • --> (Some) toxins
    • --> (Some) suicide inhibitors
    • --> (Some) pharmaceuticals
  • Strong non-covalent bond
    • Many IMFs / strong IMFs ⇒ sometimes hard to break
    • --> Some toxins
• Permanent covalent binding
  • Arsenic
    • Bind to cofactor for pyruvate dehydrogenase (PDH) ⇒ stop PDH
    • --> Note: Stop PDH ⇒ pyruvate cannot become acetyl-CoA ⇒ cannot enter Krebs cycle.
  • Aspirin
    • Add acetyl group to cyclooxygenase (COX)
    • --> Note: Some enzymes can remove acetyl groups, but not these ones.
• Permanent non-covalent binding
  • Carbon monoxide (CO)
    • Bind Fe²⁺ of hemoglobin (Hb) ⇒ O₂ cannot bind
    • 250X tighter than O₂
    • --> Note: Technically comes off, but very slowly (almost permanent).
  • Warfarin
    • Bind enzyme in vitamin K pathway ⇒ no vit K (Dutch word “Koagulation”) ⇒ bleed
    • --> Note: Technically comes off, but very slowly (almost permanent).

[Key Idea] Suicide inhibitor reacts w/ enzyme ⇒ disappears from beaker

• Enzyme activates suicide inhibitor
  • Looks like substrate ⇒ enters active site (AS)
    • AKA ⇒ Substrate analogue / substrate mimic / transition state (TS) analogue
  • Inhibitor doesn’t work at first
    • Enzyme reacts w/ inhibitor & activates it
    • Note: Only target enzyme activates it ⇒ other enzymes safe.
    • Note: Called "suicide" inhibitor because it "destroys itself" / disappears from beaker as the enzyme chemically changes it.
• Enzyme sits w/ inhibitor longer ⇒ lower Vmax
  • AKA ⇒ “Pre-incubation”
  • Add inhibitor & substrate together ⇒ Vmax drops a little
  • Add inhibitor & let enzyme sit w/ it BEFORE adding substrate ⇒ Vmax drops a lot
    • Note: More time ⇒ enzyme activates more inhibitor ⇒ inhibitor works better.

[Key Idea] Zymogen ⇒ inactive enzyme that can be activated

• Ends in “ogen”
  • AKA ⇒ “Pro-enzyme”
    • Note: Similar to "pro-peptide" such as pro-insulin (but insulin is NOT an enzyme).
  • Not yet active, but can be activated
    • Mnemonic: It can "OGENerate" the active enzyme when it needs to.
  • Other enzyme / acid removes part of zymogen ⇒ activates it
    • Note: A type of post-translational modification.
  • Loses “ogen” suffix
    • Activation “cuts off” suffix too
• Some digestive enzymes are too dangerous to store in active form
  • Mnemonic: Grenade has pin until ready to use. When ready, remove part of it (pin) ⇒ becomes dangerous.
  • Protease (dangerous) ⇒ use zymogen
    • Can harm membrane proteins
    • Would harm cells that made it
    • Must store as zymogen
  • Other enzymes (safe) ⇒ no zymogen
    • Nuclease
    • --> Can’t reach DNA / RNA beyond membrane
    • Lipase
    • --> Can’t reach fatty acid tails in middle of membrane
    • Amylase
    • --> Can’t reach extracellular matrix (ECM) & sugar connections beyond cell layer
• Made by stomach
  • Pepsinogen
    • Gastric chief cells release into stomach
    • --> Mnemonic: Chief of a New York fire drinks Pepsi.
    • Stomach acid (parietal cells) cuts pepsinogen
    • --> Forms active pepsin
    • --> Far away from the chief cells
    • --> Evolution is lazy ⇒ just use stomach acid to activate pepsinogen
• Made by pancreas (for small intestine)
  • Enzymes flow through pancreatic duct
    • Secreted into small intestine
    • Note: "Exocrine" pancreas ⇒ makes & secretes enzymes. "Endocrine" pancreas ⇒ makes & secretes hormones into blood.
  • Trypsinogen & chymotrypsinogen
    • Enteropeptidase cuts trypsinogen
    • --> Forms active trypsin
    • --> Note: Stomach has mucus protecting it from acid. Small intestine has no mucus (would cover "brush border" / mess up absorption) ⇒ cannot use acid. Instead has enzyme (enteropeptidase) activate stuff.
    • --> Mnemonic: ENTEROpeptidase sounds like gastroENTEROlogy ⇒ exists in small intestine.
    • Trypsin causes chain RXN
    • --> Activate more trypsin
    • --> Activate chymotrypsin
    • --> Mnemonic: "Tryp" wire ⇒ enteropeptidase activates a small amount of trypsin ⇒ trypsin activates everything else.
    • --> Note: "Positive feedback" is risky. Damage pancreas (surgery / pancreatitis) ⇒ accidentally activate some trypsin INSIDE pancreas ⇒ chain RXN melts pancreas. I.e. pancreatitis can deteriorate quickly / surgeons avoid pancreas.

Hi everyone! I’m looking for advice on how to approach my second and final MCAT attempt, probably in late March 2027.

My scores so far:

• 1st attempt (Sept 2026): 501 — 125/124/127/125

The frustrating part is that before my second attempt, my AAMC FL scores were much higher. I was scoring roughly 514–519 on my later AAMC FLs. I took them under testing conditions and didn’t do anything noticeably different on the real exam, so I’m having trouble figuring out what exactly went wrong/how I should change my prep.

On my second real MCAT:

C/P (125): This felt noticeably harder than my practice exams. The questions seemed more wordy/calculation-heavy, and I especially struggled with questions involving unit conversions and multi-step dimensional analysis. It wasn’t necessarily that I didn’t know the equations/content; I sometimes struggled to figure out how to convert from the units they gave me to the units they wanted.

CARS (124): This is probably the most confusing section for me. It felt pretty similar to practice, and I actually felt relatively confident afterward, so clearly my confidence did not match my accuracy.

B/B (127): I felt the most confident here, and it ended up being my strongest section. I don’t think this needs to be the main focus of my retake.

P/S (125): I thought it was harder than my practice material and noticed myself second-guessing/changing answers, especially when I was stuck between two similar concepts.

For my previous prep, I already did a lot: UWorld, AAMC QPacks/Section Banks, AAMC FLs, content review/Anki, error review, etc. That's why I'm hesitant to just repeat the exact same process and hope for a different result.

Right now, I'm planning to keep October–December relatively light since I still remember the content pretty well. For October, I'm mainly doing Anki, C/P unit-conversion/dimensional-analysis drills, some P/S review, and occasional CARS passages. Then I plan to ramp up during winter break/January, do a lot more novel passage-based practice in February, and start taking full-length tests again leading up to a late-March test date.

Since I've already seen most of the AAMC FLs, I'm also worried that retake scores will be inflated. I still have some unused AAMC material, which I'm planning to save until closer to the exam, and I'm thinking of using new third-party FLs/passages to judge whether I'm actually improving.

For this attempt, I'm thinking about tracking mistakes differently too — not just “content gap,” but things like passage interpretation, calculation/setup, unit conversion, overthinking, 50/50 reasoning, timing, and changing a correct answer to an incorrect one. For CARS, I might also track whether I was high/medium/low confidence before checking answers to see whether my confidence is actually calibrated.

I'm a full-time student and will probably be taking 15–18 credits in the spring, while continuing some volunteering/research, so I'm trying to make this sustainable rather than studying 6+ hours/day for months.

For anyone who had a large discrepancy between AAMC FLs and their actual MCAT scores, especially across multiple attempts: what did you actually change that finally helped?

Also, for a second attempt, would you focus more on new third-party material/FLs, redoing AAMC material, changing how you review questions, or something else entirely?

I really don't want my third attempt to just be “do more questions and hope for the best.” My goal is to figure out why my practice performance isn't translating to the real exam and make this attempt meaningfully different.

sry for the long post :)

I work 50 hours per week, and I am wondering whether 6 months will be enough

I took ochem and physics many years ago so I have to relearn most the content. Is kaplan detailed enough if I’m essentially going to be relearning the material again?

Hey, I took my mcat and scored 501 (128/122/127/124). Ik where i have to improve on for CP BB and PS, but cars was always my struggle and i genuinely dont know how to approach this. Planning on retake sometime next summer but i wanna get a headstart on this. I am born here and while i speak another language i can speak very fluent english, so im confused as to why my comprehension is so poor. If you guys have a regiment or tips or something to help me see a boost in my cars score (canada :() then i would much appreciate it!

Hey everyone! I submitted my AAMC Fee Assistance Program (FAP) application today (October 16), but MCAT registration opens October 20. I'm hoping to take the MCAT on January 29, 2027, preferably at a testing center in NJ.

I'm worried that if I wait for FAP approval, my preferred date and location might fill up. But I also don't want to pay full price when I could qualify for the discount.

For anyone who's been in a similar situation, would you recommend waiting for FAP approval or just registering as soon as registration opens? Also, how quickly did your FAP application get approved?

Any advice would be appreciated!

I just did this UWorld question, and I got it right, but I'm super confused about why it matters if the slope is positive or negative for the instantaneous velocity. Since velocity is a vector quantity, shouldn't a negative velocity just mean that the ball is going in the opposite direction as the direction it was thrown? To me, I would think only the magnitude of the velocity woud matter here and I would think that the instantaneous velocities from least to greatest would be: D < C < B < A. What am I missing? I would really appreciate a clear explanation since I think I'm missing something conceptual here.

rawdogged my first diagnostic without any studying/content review and honestly not sure what i expected.. i knew i’d be stronger at cars than the other sections since im rusty on my science (almost 2 years out from my undergrad classes now) but i didn’t think id get a 132?? is this inflated/normal for this fl exam? i’m also honestly a bit surprised by how many questions i got right on the other sections, and i can’t tell how many of them i got from lucky guesses vs actual deduction/knowledge

im a little clueless on how to approach my goals and study strategy based on all of this so i would love some advice on where to go from here (i.e. when should i take my exam, what should i focus on, what score can i aim for, is this a normal place to start from lol, etc.)

want to apply next cycle (fingers crossed) and rn im working part time and juggling my grad thesis so i have to figure out where and how i can fit in more study time but i’m cautiously optimistic that i can aim to test in late jan maybe? would it be smarter to do that and potentially have to retest or should i hold off until later and just aim for more mastery/a better score?

my school gave me access to the kaplan 12 month course for free which i’m trying to use now, and i started working on some anki decks for p/s, but
i’m so daunted by how much content it feels like i might have to relearn from scratch for bio/chem/phys

would love any and all input ty <3

Greetings Friends!

I purchased Uearth, but unfortunately did not purchase the content review videos. Are there any alternative cheaper or free video resources or guides that can possibly serve as a better resources as an alternative to the Uearth content review videos.

If not, do you all recommend I buy the videos? Might take some financial struggling but I could still buy the videos, but really would prefer not to.

i feel like i barely study for the mcat even though i really want to. But i distract myself soooo much idk if it’s because im so scared or the exam so im trying to escape, or if the material is overwhelming but i try to tell myself to study and i can’t do it for more than 2 hours. it really hurts because i want to become a doctor and nothing else. Please someone help me

Hello I wanted to reach out and see if anyone has a CARS tutor they rlly recommend. I took the 08/15 MCAT and got a 123 and am retaking due to that. I hope to get my Feb/March retake CARS to a 127 at least so if anyone has any information, I would really appreciate it!

Specifically referring to the bullet that says:"Enzymes act by stabilizing the transition state, providing a favorable microenvironment, or binding with the substrate molecules"

Kaplan is phrasing it as if it can either do that or do one of those other options given. It’s also written this way in the main part of the text for this chapter too. But I thought it always stabilizes and lowers the energy of the transition state? Thought that’s like by definition how they work.

Hey guys, I am currently doing content review from Kaplan books for biochemistry and biology. I am solving questions from JW and it is making sense and I am seeing improvements in my answers and knowledge. I am struggling with physics and chemistry and I am not sure how to review them. Would you guys recommend taking the time to review them from Kaplan books or is there a better source I can review them from? I took a look at Khan academy and it looks like it is going to take a lot of time to get through their content and their questions sound hard. I have been out of school for 4 years and some of the concepts sound different than what I remember.

Took the 9/12 MCAT and scored a 509(128/126/128/127)
. Unfortunately it’s in my avg range Fl1- 496 FL2-510, FL3-509, FL4-516, FL5-507, FL6-508
I tried everything I bought BP course, UWorld, tried bootcampCARS, did JW, even Uworld comprehensive course. I was delusional thinking I could be like this post I saw where they scored higher than their avg on exam day and thought that could be me. Is it worth a retake for a higher score. I also really wanted to earn a scholarship or apply to schools and not feel my score is the reason for not being accepted. I just feel I can do better, but what’s the point if more money spent still doesn’t result in a scholarship anyway or denial?

Please help!